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Trental (Pentoxifylline)

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Generic Trental is used for treating intermittent claudication (pain, cramping, numbness, or weakness in the foot, hip, thigh, or buttocks) in certain patients. It may also be used for other conditions.

Other names for this medication:

Similar Products:
Pletal, Pentoxil


Also known as:  Pentoxifylline.


Generic Trental is used for treating intermittent claudication (pain, cramping, numbness, or weakness in the foot, hip, thigh, or buttocks) in certain patients. It may also be used for other conditions.

Generic Trental is a xanthine derivative blood flow enhancer. It works by thinning the blood and improving red blood cell flexibility, causing the blood to flow more freely through the veins.

Trental is also known as Pentoxifylline.

Generic name of Generic Trental is Pentoxifylline.

Brand name of Generic Trental is Trental.


Take Generic Trental by mouth with food or milk.

Swallow whole. Do not break, crush, or chew before swallowing.

If you want to achieve most effective results do not stop taking Generic Trental suddenly.


If you overdose Generic Trental and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children in a container that small children cannot open.

Side effects

The most common side effects associated with Trental are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Generic Trental if you are allergic to Generic Trental components, or to methylxanthines (theophylline, caffeine, theobromine).

Be very careful with Generic Trental if you are pregnant, planning to become pregnant. Generic Trental is found in breast milk. Do not breast-feed while taking Generic Trental.

Do not take Generic Trental if you have had recent bleeding in the brain or eye.

Tell your health care provider or dentist that you take Generic Trental before you receive any medical or dental care, emergency care, or surgery.

It may take 2 to 4 weeks to notice improvement in your condition, and up to 8 weeks for maximum relief.

Use Generic Trental with caution in the elderly. They may be more sensitive to its effects.

Avoid alcohol.

Avoid machine driving.

It can be dangerous to stop Generic Trental taking suddenly.

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4 groups (n = 6/group) received 30 ng of Escherichia coli O55:B5 endotoxin/kg of body weight, i.v., over 30 minutes, and 1 of the following preparations 15 minutes before and 8 hours after endotoxin infusion: FM, 1.1 mg/kg; PTX, 8 mg/kg; FM/PTX, 1.1 mg of FM and 8 mg of PTX/kg; and saline solution bolus (ENDO). Clinical and hematologic variables were measured over 24 hours.

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Two review authors independently abstracted information for the outcomes of interest. Typical relative risk (RR) and risk difference (RD) with 95% confidence intervals (CI) using fixed effects model are reported for dichotomous outcomes and mean differences for continuous outcomes. NNT was calculated for outcomes for which there was a statistically significant reduction in RD.

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Administration of pentoxifylline improved RBC deformability of horses at rest and during treadmill exercise.

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Compounds suppressing the production of tumor necrosis factor-alpha are protective in animal models of septic shock. Recent studies demonstrated a beneficial effect of xanthine derivatives, which suppress tumor necrosis factor-alpha production by acting as non-specific cAMP phosphodiesterase inhibitors. In this experiment we tested the effect of (+/-)-rolipram (racemate) and its enantiomers on human mononuclear cells stimulated with lipopolysaccharide (LPS). Rolipram has a phenyl-pyrrolidinone structure, unrelated to the methylxanthines, and acts as a specific inhibitor of the type IV phosphodiesterase. Our results identify rolipram as a remarkably potent suppressor of the LPS-induced synthesis of tumor necrosis factor-alpha. When compared to the non-specific inhibitor pentoxifylline, the IC50 of (+/-)-rolipram (130 nM) is more than 500 times lower. The influence of rolipram on tumor necrosis factor-alpha production depended on the steric configuration of the molecule, since the (-)-enantiomer exhibited a five times lower IC50 than the (+)-enantiomer. The inhibitory effect of all substances tested is selective for tumor necrosis factor-alpha rather than interleukin-1 beta, since interleukin-1 beta production is only slightly influenced.

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The phosphodiesterases inhibitor pentoxifylline gained attention for Duchenne muscular dystrophy therapy for its claimed anti-inflammatory, antioxidant, and antifibrotic action. A recent finding also showed that pentoxifylline counteracts the abnormal overactivity of a voltage-independent calcium channel in myofibers of dystrophic mdx mice. The possible link between workload, altered calcium homeostasis, and oxidative stress pushed toward a more detailed investigation. Thus a 4- to 8-wk treatment with pentoxifylline (50 mg x kg(-1) x day(-1) ip) was performed in mdx mice, undergoing or not a chronic exercise on treadmill. In vivo, the treatment partially increased forelimb strength and enhanced resistance to treadmill running in exercised animals. Ex vivo, pentoxifylline restored the mechanical threshold, an electrophysiological index of calcium homeostasis, and reduced resting cytosolic calcium in extensor digitorum longus muscle fibers. Mn quenching and patch-clamp technique confirmed that this effect was paralleled by a drug-induced reduction of membrane permeability to calcium. The treatment also significantly enhanced isometric tetanic tension in mdx diaphragm. The plasma levels of creatine kinase and reactive oxygen species were both significantly reduced in treated-exercised animals. Dihydroethidium staining, used as an indicator of reactive oxygen species production, showed that pentoxifylline significantly reduced the exercise-induced increase in fluorescence in the mdx tibialis anterior muscle. A significant decrease in connective tissue area and profibrotic cytokine transforming growth factor-beta(1) was solely found in tibialis anterior muscle. In both diaphragm and gastrocnemius muscle, a significant increase in neural cell adhesion molecule-positive area was instead observed. This data supports the interest toward pentoxifylline and allows insight in the level of cross talk between pathogenetic events in workloaded dystrophic muscle.

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PTX does influence neither liver injury nor early profibrogenic events in the CDD model of NASH.

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 C-reactive protein (CRP) is increased among patients on maintenance hemodialysis. Such inflammatory markers can result in protein-energy deficit syndromes and low adequacy of dialysis in these patients. This study evaluated the effect of pentoxifylline on serum CRP level and KT/V in end-stage renal disease patients on maintenance hemodialysis.

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Oxygen exposure plays an important role in the pathogenesis of bronchopulmonary dysplasia (BPD). The phosphodiesterase inhibitor pentoxifylline (PTX) has anti-inflammatory and antifibrotic effects in multiple organs. It was hypothesized that PTX would have a protective effect on hyperoxia-induced lung injury (HILI).

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Previous reports have shown beneficial effects of pentoxifylline (PTX) and hypertonic saline (HS) in the treatment of hemorrhagic shock. We compared the effects of these solutions to those of conventional lactated Ringer's (LR) treatment on bacterial translocation (BT), lung injury and total and differential cell count in the bronchoalveolar lavage fluid (BAL) after hemorrhagic shock. Rats (280-330 g) were bled to a MAP of 35 mmHg for 1 h and then randomized into 4 groups: LR (3x shed blood); HS (7,5% NaCl, 4 mL/kg); LR+PTX (25 mg/kg) and SHAM (no shock, no treatment). Additionally, total shed blood was reinfused. At 24 h lung injury was analyzed by a pathologist blinded to the groups, and a score was calculated. BT was determined by microbiological cultures of mesenteric lymph node complex. BAL was performed on a separate set of animals that received the same treatments. Lung score was significantly higher in LR group (11.5+/-1.4) as compared to HS (6.8+/-0.9), and PTX treated animals (7.2+/-0.9). The percentage of neutrophils in the BAL of LR animals (15.8%) was also significantly higher as compared with HS (5.25%) and PTX groups (9.72%). BT was noted in 50% of rats for LR group, 30% for PTX, 10% for HS and 0% for sham group. HS and PTX reduced BT and lung injury after hemorrhage. Attenuation of lung injury could be the result of less neutrophil infiltration into the lungs of HS and PTX treated animals. LR resuscitation caused pronounced lung injury and BT.

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We sought to determine whether local administration of pentoxifylline (PTF) or propentofylline (PPTF), which hinders cytokine production, influences pain threshold and formalin-induced pain behavior in rats or the level of tumor necrosis factor-alpha (TNF-alpha) messenger RNA (mRNA) concentrations in the inflamed paw tissue. PTF (0.5, 1, or 2 mg) and PPTF (1 or 2 mg) injected intraplantarly ( had no significant effect on pain threshold. Injection of 0.1 mL of a 12% formalin solution subcutaneously into the dorsal surface of the left hindpaw induced pain behavior (47.6 +/- 4.6 incidents per 5 min), and PTF injected at doses of 1 and 2 mg/100 microL before (but not after) formalin was effective in antagonizing (33.6 +/- 2.5 and 23.6 +/- 3.4 incidents per 5 min, respectively) formalin-induced pain behavior. A similar antagonistic effect was observed after PPTF treatment at a dose of 2 mg/100 microL; however, in contrast to PTF, at a later time point (85-90 min) after the formalin challenge, this effect was independent of the scheme of PPTF administration, before or after formalin. The effect of PTF on formalin-induced pain behavior did not parallel paw volume as measured by plethysmometer; however, PTF per se significantly increased the paw volume. Formalin injection significantly increased the TNF-alpha mRNA level in the inflamed tissue of the rat hind paw (150%). PTF administered before, but not after, formalin significantly antagonized (by approximately 40%) the observed increase in the level of TNF-alpha mRNA. Our study demonstrates and provides biochemical evidence that preemptive inhibition of proinflammatory cytokine synthesis by the use of PTF and PPTF, phosphodiesterase, and glial activation inhibitors is useful in antagonizing hyperalgesia in formalin-induced pain. Moreover, local administration of PTF may be a valuable approach to the treatment of inflammatory pain.

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The effect of intracellular cAMP rise on nitric oxide (NO) production was compared in murine primary fibroblasts isolated from the spleens of CBA mice, and L929 fibrosarcoma cell line. Treatment of confluent L929 cells with cAMP analogues -dibutyryl-cAMP (db-cAMP) or 8-Cl-cAMP caused dose-dependent augmentation of inducible NO synthase (iNOS)-mediated NO production, which has been abrogated by inhibition of protein synthesis with cycloheximide or addition of selective iNOS inhibitor aminoguanidine. In contrast, under the same cultivating conditions, cAMP analogues were not able to upregulate NO synthesis in primary fibroblasts. Treatment with cAMP analogues or non-selective phosphodiesterase (PDE) inhibitor pentoxifylline affected IFNgamma-induced NO synthesis in both cell types, but in the opposite manner-enhancing in L929 cells and suppressive in primary fibroblasts. The induction of iNOS, but not its catalytic activity, was impaired in cAMP-treated primary fibroblasts. Finally, PDE type IV inhibitor rolipram enhanced IFN-gamma-triggered NO synthesis in L929 cells, but was unable to mimic cAMP analogue or PTX-mediated suppression of NO synthesis in spleen fibroblasts. These results suggest that, in contrast to L929 fibrosarcoma cell line, intracellular cAMP rise might have a role in downregulation of NO production in murine primary fibroblasts.

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The administration of pentoxifylline reduced the transforming growth factor β-marked area and the amount of transforming growth factor β expressed in liver tissue. This effect was not observed after the administration of prednisolone. There was a significant reduction in vascular endothelial growth factor expression after the administration of either drug compared with the non-treatment group.

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Monocrotaline (MCT) is a pyrrolizidine alkaloid (PA) plant toxin that causes hepatotoxicity in humans and animals. Human exposure occurs from consumption of contaminated grains and herbal teas and medicines. Intraperitoneal injection (i.p.) of 300 mg/kg MCT in rats produced time-dependent hepatic parenchymal cell (HPC) injury beginning at 12 h. At this time, an inflammatory infiltrate consisting of neutrophils (PMNs) appeared in areas of hepatocellular injury, and activation of the coagulation system occurred. PMN accumulation was preceded by up-regulation of the PMN chemokines cytokine-induced neutrophil chemoattractant-1 (CINC-1) and macrophage inflammatory protein-2 (MIP-2) in the liver. The monocyte chemokine, monocyte chemoattractant protein-1 (MCP-1), was also upregulated. Inhibition of Kupffer cell function with gadolinium chloride (GdCl(3)) significantly reduced CINC-1 protein in plasma after MCT treatment but had no effect on hepatic PMN accumulation. Since inflammation can contribute to either pathogenesis or resolution of tissue injury, we explored inflammatory factors as a contributor to MCT hepatotoxicity. To test the hypothesis that PMNs contribute to MCT-induced HPC injury, rats were depleted of PMNs with a rabbit anti-PMN serum prior to MCT treatment. Anti-PMN treatment reduced hepatic PMN accumulation by 80% but had no effect on MCT-induced HPC injury or activation of the coagulation system. To test the hypothesis that Kupffer cells and/or tumor necrosis factor-alpha (TNF-alpha) are required for MCT-induced HPC injury, rats were treated with either GdCl(3) to inhibit Kupffer cell function or pentoxifylline (PTX) to prevent synthesis of TNF-alpha. Neither treatment prevented MCT-induced HPC injury. Results from these studies suggest that PMNs, Kupffer cells and TNF-alpha are not critical mediators of MCT hepatotoxicity. Accordingly, although inflammation occurs in the liver after MCT treatment, it is not required for HPC injury and possibly occurs secondary to hepatocellular injury.

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Rejection episodes were validated as the only independent risk factor for graft loss in this study. We compared graft survival rates in each group according to the presence or absence of acute rejection. Acute rejection reduced graft survival in the control group (graft survival rate at 1 year, 59% vs. 97%, P < 0.001), but this adverse effect was blunted in the PTX group (72% vs. 89%, NS). This improvement was confirmed by multivariate analysis for risk factors, with graft survival rates being described at best as the interaction between rejection and treatment (PTX vs. placebo, P = 0.045).

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Maternal infection is a cause of adverse developmental outcomes. Lipopolysaccharide (LPS)-induced embryonic resorption, intra-uterine fetal death (IUFD) and preterm labor have been well characterized. In the present study, we investigated the effects of maternal LPS exposure on intra-uterine fetal growth and skeletal development. All pregnant mice except controls received an intraperitoneal injection of LPS (75 microg/kg) on gestational days (GD) 15-17. The number of live fetuses, dead fetuses and resorption sites was counted on GD 18. Live fetuses in each litter were weighed. Crown-rump and tail lengths were examined and skeletal development was evaluated. As expected, perinatal LPS exposure resulted in 63.2% fetal death. LPS significantly lowered fetal weight, reduced crown-rump and tail lengths, and retarded skeletal ossification in caudal vertebrae, anterior and posterior phalanges, and supraoccipital bone. Additional experiment showed that a single dose of LPS (75 microg/kg, i.p.) on GD 15 increased the expression of TNF-alpha mRNA in maternal liver and placenta and TNF-alpha concentration in maternal serum and amniotic fluid. Furthermore, pentoxifylline, an inhibitor of TNF-alpha synthesis, significantly inhibited TNF-alpha production, reduced fetal mortality, and reversed LPS-induced fetal intra-uterine growth restriction and skeletal development retardation. Taken together, these results suggest that TNF-alpha is, at least in part, involved in LPS-induced intra-uterine fetal death, intra-uterine growth restriction and skeletal development retardation.

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To examine the effect of pentoxifylline (PTX) on cytokine levels, lipid peroxidation, and antioxidant enzymes in a rabbit model of spinal cord ischemia-reperfusion injury induced by aortic occlusion.

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The tumor-infiltrating macrophage density correlated significantly and positively with tumor IL-8 mRNA expression and intratumor microvessel counts and significantly and negatively with patient survival. In addition, after cell-cell interaction in cancer cell:macrophage cocultures, marked IL-8 mRNA expression was induced in lung cancer cells (approximately 270-fold) and, to a lesser degree, in macrophages (4.5-fold). The increase in IL-8 mRNA expression correlated with the in vitro metastatic potential of the cancer cells. All six anti-inflammatory agents suppressed induction of IL-8 mRNA expression in lung cancer cells by >90%, four (pentoxifylline, celecoxib, pyrrolidine dithiocarbamate, and dexamethasone) having a dose-dependent effect. NF-kappaB transcriptional regulation and protein levels were simultaneously increased in the nuclei of cancer cells in macrophage/cancer cell cocultures, this effect also being suppressed by all six anti-inflammatory agents.

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Rats that received pig serum showed significant liver fibrosis, and their serum interleukin-6 (IL-6) and hyaluronic acid levels were significantly increased. The serum levels of IL-6 were well correlated with the serum levels of hyaluronic acid, and increased as the liver fibrosis progressed. Penoxifylline prevented the development of fibrosis in this animal model and reduced the serum levels of IL-6 in a dose-dependent manner. In vitro, by the addition of PTX to the culture medium of the rat hepatic stellate cells (HSCs), the proliferation of the HSCs was significantly inhibited and IL-6 in the culture supernatant was also reduced significantly. Exogenous addition of IL-6 partially restored the proliferation.

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Without immunosuppressants and insulin, the LSF-treated recipient mice maintained euglycemia significantly longer than the saline-treated recipients (mean, >65 days in the LSF-treated group vs. 6 days in saline controls; P=0.0004). Serum levels of interferon-gamma were markedly reduced in LSF-treated recipients at 1 and 3 weeks posttransplant. Diabetes recurred in the LSF-treated recipients after removing the islet-implanted kidneys. Immunohistochemistry showed retention of insulin-positive cells in the grafts of the LSF-treated recipients. LSF preserved beta-cell insulin secretory function in the presence of inflammatory cytokines in vitro.

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Portal vein ligation produced significant increments in liver enzymes, NO, creatinine and portal pressure concomitant with significant decrements in glutathione content and superoxide dismutase activity. Treatment with captopril, PTX, and C. sinensis resulted in a significant reduction in liver enzymes, NO, creatinine and portal pressure and observable increase in antioxidant enzymes.

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Intraoperative vasospasm during reconstructive microsurgery is common, often unpredictable, and potentially devastating with regard to flap survival. Current methods of pharmacologic management vary, and may be shifting as a result of changes in the availability of individual medications. This review aims to provide a concise examination of the published literature regarding use, efficacy, and adverse effects of the agents described for local management of vascular spasm during microsurgery.

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Pentoxifylline (PTX), a methylxanthine derivative, was examined for its effects on T cell proliferation and cytokine production stimulated by cross-linking anti-CD3 alone, anti-CD3 with PMA, anti-CD3 with anti-CD26, or anti-CD3 with anti-CD28 mAb, respectively. PTX at a 3.5 x 10(-5) M concentration significantly inhibited T cell proliferation and the production of tumor necrosis factor-alpha, interleukin-2, and interleukin-4. Moreover, this effect was selective for stimulation by cross-linking anti-CD3 with PMA, or anti-CD3 with anti-CD26, but not by cross-linking anti-CD3 with anti-CD28. These results suggest that the inhibitory effect of PTX on T cell activation involves the CD3 and CD26, but not the CD28 signal pathway.

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The study was designed to study the effect of pentoxifylline PTX on the chemiluminescence responses of neutrophils and on tumor necrosis factor-alpha (TNF-alpha)-induced priming of neutrophils. The results demonstrate that TNF-alpha stimulated the respiratory burst by neutrophils and primed them for enhanced response to fMLP but not to PMA. The effect of TNF-alpha on the oxygen metabolism of neutrophils was inhibited when cells were treated with PTX. This reaction was dose-dependent. Additionally, the inhibiting influence of PTX on the chemiluminescence response of neutrophils was observed.

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Extensive apoptosis or programmed cell death (PCD) of both hematopoietic (erythroid, myeloid, megakaryocytic) and stromal cells in myelodysplastic syndromes (MDS) cancels the high birth-rate resulting in ineffective hematopoiesis and has been demonstrated as the probable basis for peripheral cytopenias in MDS by our group. It is proposed that factors present in the microenvironment are inducing apoptosis in all the cells whether stromal or parenchymal. To investigate this hypothesis further, bone marrow biopsies from 46 MDS patients and eight normal individuals were examined for the presence of three cytokines, tumor necrosis factor-alpha (TNF-alpha), transforming growth factor-beta (TGF-beta) and granulocyte macrophage-colony stimulating factor (GM-CSF) and one cellular component, macrophages, by the use of monoclonal antibodies immunohistochemically. Results showed the presence of TNF-alpha and TGF-beta in 41/46 and 40/46 cases of MDS respectively, while only 15 cases showed the presence of GM-CSF. Further a significant direct relationship was found between the degree of TNF-alpha and the incidence of PCD (p= 0.0015). Patients who showed high PCD also had an elevated TNF-alpha level. Thus, the expression of high amounts of TNF-alpha and TGF-beta and low amounts of the viability factor GM-CSF may be responsible for the high incidence of PCD leading to ineffective hematopoiesis in MDS. Future studies will be directed at attempting to reverse the lesion in MDS by using anti-TNF-alpha drugs such as pentoxifylline.

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In 5 level 2 studies, physical training increased pain-free and total walking distance significantly (139.0 m [95% confidence interval {CI}, 31.0 to 246.9 m] and 179.1 m [95% CI, 60.2 to 298.1 m], respectively). In a level 3 study, smoking cessation resulted in a nonsignificant increase in total walking distance of 46.7 m (95% CI, -19.3 to 112.7 m). In 6 level 1 studies, pentoxifylline increased both pain-free and total walking distance by 21.0 m (95% CI, 0.7 to 41.3 m) and 43.8 m (95% CI, 14.1 to 73.6 m), respectively. In 4 level 1 trials, nafronyl significantly increased pain-free walking distance (58.6 m [95% CI, 30.4 to 86.8 m]) and total walking distance (71.2 m [95% CI, 13.3 to 129.0 m]).

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Matrix metalloproteinase inhibitors (MMPIs) reduce blood-brain barrier (BBB) disruption and prevent cell death. Animal models of multiple sclerosis, cerebral ischemia and hemorrhage, and bacterial meningitis respond to treatment with MMPIs. We have used the intracerebral injection of lipopolysaccharide (LPS) in rat, which induces MMP production and results in a delayed opening of the BBB, to screen MMPIs to identify therapeutic agents. We hypothesized that the mouse would respond similarly to LPS and that the mouse/LPS model of BBB damage would be more useful for screening of MMPIs. Therefore, we adapted the rat LPS model to the mouse and compared the response to LPS and treatment with MMPIs. Wistar-Kyoto rats (WKY) and three strains of mice had stereotactic injections of LPS into the caudate. (14)C-sucrose was used to measure permeability of the BBB 24 h after injection. Initially, we tested three broad-spectrum MMPIs in the rat, BB-1101, BB-94, and BB-2293, and a MMP-2 selective inhibitor, IW449; both BB-1101 and BB-94 significantly suppressed LPS-induced BBB damage (p<0.05). In the 3 mouse strains, C57/BL6, C57/BL10, and C57/BL10HIIIR2, LPS significantly opened the BBB in C57/BL6, and it was the only strain that showed a reduction in BBB permeability with BB-94. Treatment with methylprednisolone and several broad-spectrum MMPIs, including BB-1101, was ineffective in the C57/BL6. There was a significant reduction in BBB permeability seen with 10% dimethyl sulfoxide (DMSO) alone, which was used to dissolve the selective MMP-2 and-9 inhibitor, SB-3CT. The tetracycline derivative, minocycline, reduced the BBB injury in mouse by blocking the production of MMP-9. Our results show variability in rats and mice to LPS and MMPIs, which most likely is based on genetic make-up. Understanding these differences may provide important clues that could guide selection of MMPIs in treatment of neurological diseases.

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Pentoxifylline can inhibit blood leukocyte functions in vitro, and some inflammatory processes in the lung in vivo. Therefore, we examined the effects of pentoxifylline on alveolar macrophage functions in vitro. Alveolar macrophages were harvested from normal rat lungs by airway lavage. The dose-response relationship of varying concentrations of pentoxifylline and in vitro cell functions were examined. Macrophage functions studied included adherence to nylon wool, random (unstimulated) and zymosan-activated serum-stimulated migration through 5 microns millipore filters, and superoxide generation induced by zymosan-activated serum as assayed by cytochrome c reduction.

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The aim of the present study was to develop a reproducible autogenic model-based method for collection, conservation and isolation of porcine pancreas so that transplantation of isolated pancreatic islets could be performed and postoperative normoglycemia achieved.

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The deformability of red blood cells (RBC) is one of the factors that determine whole blood rheology. Derivatives of vitamin K (phytomenadione, menadione, menadione bisulfite) are electron-transporting substances. The aim of this study was to investigate the possible influence of derivatives of vitamin K on erythrocyte deformability in studies in vivo--on rats and rabbits. The influence of vitamin K antagonist on erythrocyte deformability (ethylbiscumacetate) was also determined. Pentoxifylline known to affect RBC deformability was also included in the study as the control treatment. The study was performed on white laboratory rats and domestic rabbits. The blood was obtained from animals after single and multiple dosing of drugs. Blood sample was prepared and RBC filterability was assayed with a gravity driven filtration technique. Pentoxyfylline did not change erythrocyte deformability after single dose, but significantly improved erythrocyte deformability of laboratory animals after multiple application. Filterability values of the RBCs of the rats and rabbits increased significantly after single and multiple treatment with phytomenadione, while the two other derivatives, menadione and menadione bisulfite, did not change RBC deformability. Ethylbiscumacetate did not change erythrocyte deformability in rats after single dose.

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A sensitive and selective liquid chromatographic-electrospray ionization mass spectrometric method for the simultaneous determination of propentofylline and enantiomers of its active metabolite M1 in rat serum, cortex and hippocampus was developed and validated according to GLP procedures. Sample preparations were carried out by liquid-liquid extraction using diethyl ether after the addition of the internal standard (pentoxifylline). The dried residue was reconstituted in mobile phase and injected onto a Chiralpak AD column (10 µm, 250 × 4.6 mm i.d.). The limit of quantification for propentofylline in serum, cortex and hippocampus was set at 0.25 ng/mL and for enantiomers of its metabolite M1 at 1.25 ng/mL. The established LC/ESI-MS/MS method has been successfully applied to an initial pharmacokinetic study of propentofylline and also to assessment of distribution of parent drug and enantiomers of its pharmacologically active metabolite M1 to cortex and hippocampus after intravenous administration of propentofylline to rats at a dose of 5 mg/kg.

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The pentoxifylline influence on neutral proteinase, alpha-2-macroglobulin, trypsin-alpha-1-proteinase inhibitor and elastaseinhibitory activity under cycloheximide injection has been investigated. Two hours after cycloheximide injection the activity of neutral buy trental proteinases increases in rats serum, lungs, heart, liver and kidneys. The preliminary injection of pentoxifylline prevents increase of neutral proteinases activity. Cycloheximide also decreases alpha-2-macroglobulin activity in serum and liver and trypsin-, elastaseinhibitory activity of alpha-1-proteinase inhibitor in all investigated organs. At using pentoxifylline the alpha-2-macroglobulin activity doesn't change in liver and increases in serum in comparison with only cycloheximide and there are no observed any alpha-1 inhibitor proteinase activity changes in rats serum and organs.

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The reviewers searched the Cochrane Peripheral Vascular Diseases Group trials register, Embase, reference lists of relevant articles, and buy trental contacted principal investigators of trials.

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The commonly used beverage and psychostimulant buy trental caffeine is known to inhibit human acetylcholinesterase enzyme. This pharmacological activity of caffeine is partly responsible for its cognition enhancing properties. However, the exact mechanisms of its binding to human cholinesterases (acetyl and butyrylcholinesterase; hAChE and hBuChE) are not well known. In this study, we investigated the cholinesterase inhibition by the xanthine derivatives caffeine, pentoxifylline, and propentofylline. Among them, propentofylline was the most potent AChE inhibitor (hAChE IC₅₀=6.40 μM). The hAChE inhibitory potency was of the order: caffeine (hAChE IC₅₀=7.25 μM)50 μM) relative to the reference agent donepezil (hBuChE IC₅₀=13.60 μM). Molecular modeling investigations indicate that caffeine binds primarily in the catalytic site (Ser203, Glu334 and His447) region of hAChE whereas pentoxifylline and propentofylline are able to bind to both the catalytic site and peripheral anionic site due to their increased bulk/size, thereby exhibiting superior AChE inhibition relative to caffeine. In contrast, their lack of hBuChE inhibition is due to a larger binding site and lack of key aromatic amino acids. In summary, our study has important implications in the development of novel caffeine derivatives as selective AChE inhibitors with potential application as cognitive enhancers and to treat various forms of dementia.

trental pentoxifylline tablets 2016-08-09

Introduccion. Las alucinaciones musicales son un tipo de alucinacion auditiva prevalente en la poblacion no psiquiatrica, pero escasamente comunicada en la bibliografia neurologica. Ocurren con mayor frecuencia en la poblacion anciana, del sexo femenino y con perdida de audicion, pero su fisiopatologia esta por desentrañar. Casos clinicos. Se presentan seis casos (cinco mujeres y un hombre) de alucinaciones musicales diagnosticados en una consulta de neurologia general en un lapso de tiempo de cinco años. En cinco de ellos concurria la hipoacusia en mayor o menor grado y uno estaba desencadenado por la pentoxifilina. En su mayoria, el contenido musical de las alucinaciones provenia de experiencias musicales vividas en la infancia y juventud. En los casos sometidos a tratamiento farmacologico la respuesta fue pobre; sin embargo, una vez explicada a los pacientes la benignidad del cuadro y su desvinculacion con patologia psicotica, el grado de aceptacion del sintoma fue bueno. Conclusiones. Las alucinaciones musicales son una patologia fronteriza entre la neurologia, la otorrinolaringologia y la psiquiatria poco conocida, que, con frecuencia, se vincula erroneamente a la enfermedad mental. Es fundamental explicar a pacientes y familiares el caracter no necesariamente psiquiatrico de este sintoma, asi como conocer buy trental la potencialidad que tienen algunos farmacos de uso comun para generarlo.

trental renal dosing 2017-08-24

HEB can increase the contents of PAF, TXB2, PGI2, P-selectin, E-selectin, L-selectin, the ratio of TXB2 to PGI2, and the buy trental number of adhered leukocyte, as well as decrease the skin microcirculatory perfusion value. PTX can inhibit the aggregation and adhesion of platelets and leukocytes through increasing the content of PGI2 and decreasing contents of other factors mentioned above, thus alleviating the microcirculatory dysfunction after HEB.

trental suspension 2015-03-05

The progression of cells from G2 into mitosis is mainly controlled by formation of the cyclin B1/p34cdc2 complex. The behaviour of this complex in the irradiation-induced G2 cell cycle delay is still unclear. A prior study demonstrated that the expression of the cyclin B1 protein is reduced by irradiation, and restored to control levels by the methylxanthine drug pentoxifylline, which is a potent G2 block abrogator. The present study shows that irradiation, and 2 mM pentoxifylline affect the expression of the cyclin-dependent kinase p34cdc2 in HeLa cells. Irradiation induces p34cdc2 levels to increase and cyclin B1 levels to decrease. Addition of pentoxifylline at the G2 maximum reverses these trends. This is also evident from the cyclin B1/p34cdc2 ratios which decline after irradiation and are rapidly restored to control levels upon addition of pentoxifylline. It is concluded that cyclin BI and p34cdc2 protein expression are important events buy trental and act in concert to control the irradiation induced G2 block. Analysis of cyclin B1 expression in whole cells and in isolated nuclei furthermore show that cyclin B1 is translocated from the nucleus into the cytoplasm when the G2 block is abrogated by pentoxifylline.

trental generic name 2015-08-29

Pentoxifylline was subjected to various stress conditions and degradation profile was studied with conventional LCMS. Interestingly, under oxidative stress conditions the drug substance underwent distinct transformation to give rise to a single major degradation product. The structure of this product was elucidated using 1D, 2D NMR spectroscopy, high resolution mass spectrometry (Q-TOF LC/MS) and found to be a novel gem-dihydroperoxide, namely 1-(5,5-Bis-hydroperoxy-hexyl)-3,7-dimethyl-3,7-dihydro-purine-2,6-dione. An efficient stability indicating buy trental liquid chromatographic separation method was developed for pentoxifylline and its three degradation products (including two from base hydrolysis) using 1.8 microm, C18 reverse phase column and UHPLC. Baseline separation was achieved with a run time of 4 min. The analytical assay method was validated with respect to system suitability, specificity, linearity, range, precision, accuracy and robustness.

trental drug interactions 2016-08-19

An in vitro system was developed to study HIV-1 replication in freshly HIV buy trental -1-infected peripheral blood mononuclear cells (PBMC) incubated with whole azide-killed C. neoformans.

trental 250 mg 2015-01-29

Anemia is a frequent condition in patients with chronic kidney disease due to a reduction in the production of erythropoietin. Patients with inflammation respond buy trental less well to treatment with erythropoietin, possibly because the increased production of hepcidin reduces the availability of iron for hematopoiesis. Some studies suggest that pentoxifylline has anti-inflammatory properties and could be used as adjuvant therapy in the treatment of anemia.

trental and alcohol 2016-03-23

Gentamicin (GM) is a widely used antibiotic buy trental against serious and life-threatening infections, but its usefulness is limited by the development of nephrotoxicity. Thus, the present study was undertaken to determine if pentoxifylline could protect the kidney in this experimental model. Thirty male Wistar rats were used. The animals were divided into three groups, each with 10 animals. The GM group of animals was treated daily with gentamicin in a dose of 100 mg/kg for eight days. The GMP group of animals was treated daily with pentoxifylline in a dose of 45 mg/kg and the same dose of gentamicin as the GM group for eight days. The control group received 1 mL/day saline intraperitoneally. For histological analysis, 5 microm-thick sections were stained with hematoxylin and eosin (HE), periodic acid Schiff (PAS), and Jones methenamine silver. The morphometric parameters included were glomerular area, major and minor axis, perimeter, diameter, roundness, and mean optical density. Biochemical analyses were used to determine concentrations of blood urea, serum creatinine, sodium, and potassium. In the GM group of rats, glomerular basement membrane was diffusely and unequally thickened with polymorphonuclear leukocyte infiltration, and coagulation-type necrosis and vacuolization of cytoplasm of proximal tubules epithelial cells were observed. In the GMP group of rats, glomeruli were slightly enlarged with thickened basement membrane in some segments but without coagulation-type necrosis of proximal tubules epithelial cells. Blood urea and serum creatinine concentration in the GM group were significantly elevated in comparison with the GMP group, while the potassium level was decreased. The present study indicated that pentoxifylline could provide a marked protective effect against gentamicin-induced acute renal failure, most likely mediated by vascular decongestion.

trental 100 mg 2017-03-26

This investigation was conducted as a randomized clinical trial incorporating a control group (Standard drug group SDG, multivitamin, and local heat therapy) in comparison to buy trental pentoxifylline test cases (Experimental drug group EDG, 400mg 3 times daily, as coated, sustained release tablets). The stipulated treatment period was 7 months and a total of 29 cases of advanced fibrosis (14 test subjects and 15 age and sex matched diseased controls) were included in this study and 100% compliance was reported at the end ofthe test period.

trental 600 mg 2017-07-29

The analyses of treatment buy trental results in 82 patients with general purulent peritonitis are presented. In these patients long-term intraarterial catheter therapy (IACT) was included in the complex of postoperative treatment after elimination of infection source. Postoperative peritonitis was in 66 patients, 52 patients of them underwent reoperations for persisting general peritonitis. Use of IACT promoted arrest of abdominal inflammatory process and polyorganic insufficiency due to high concentration of antibiotics in the affection focus, improvement of regional circulation, reduced number of postoperative complications and a sharp fall of lethality of 8.5%.

trental 400 dosage 2016-09-26

To study the effect of pentoxifylline (PTX) on the content of hepatic TGF-beta 1, type I and type III collagen in schistosome-infected buy trental mice with liver fibrosis.

trental dosing 2015-02-11

The instillation of HCl (pH 1.25, 1.2 ml/kg) into the right lung resulted in an increase in the protein permeability of the right lung's alveolar epithelium and endothelium as well as an increase in the permeability to protein of the left lung's endothelium. Pentoxifylline pretreatment attenuated the increase in the endothelial permeability of both lungs by 50% and restored the PaO2/FIO2 to normal in the pretreated animals exposed to buy trental acid injury.

trental medication dosage 2016-10-19

The goal of this study was to confirm or rule out anecdotal reports of beneficial effects of clonidine and pentoxifylline in the treatment of painful diabetic peripheral neuropathy. Clonidine was administered to 16 subjects at two dosage levels (0.1 and 0.2 mg/day) and was compared to placebo in a crossover design Propecia Reviews , with each phase lasting 4 wk. Either pentoxifylline (400 mg 3 times/day) or placebo was given to 21 subjects in a 12-wk trial. Discomfort was characterized and rated with a subjective pain score (range 0-20). There was a significant decrease in pain score from baseline with both active drugs (P less than 0.05), but this was no better than the response to placebo (P less than 0.30 for clonidine and P less than 0.95 for pentoxifylline). This study does not demonstrate a short-term benefit of either clonidine or pentoxifylline in the treatment of peripheral neuropathy.

trental 50 mg 2017-09-13

Digital ischemia with gangrene of one or several fingertips has been described as a paraneoplastic syndrome associated with various malignant tumors, especially adenocarcinomas. Most often this paraneoplastic syndrome represents the first symptom of an occult neoplasia in an advanced stage. We present the case of an 83 year-old patient with digital ischemia and gangrenous fingertips in association with a latent adenocarcinoma of the uterus and metastatic involvement of the paraaortal lymph nodes. Acute occurrence of digital ischemia and gangrene without pathological laboratory Sinemet Maximum Dosage findings and negative past medical history concerning cardiovascular-induced emboli, arteriosclerotic occlusion, or rheumatologic and autoimmune diseases should suggest this paraneoplastic syndrome and lead to thorough search for an underlying tumor.

trental overdose 2015-12-13

Tissue factor (TF), the membrane glycoprotein that initiates blood coagulation, is constitutively expressed by many tumor cells and is implicated in peri-tumor fibrin deposition and hypercoagulability in cancer. Upregulation of tumor TF correlates with enhanced metastatic potential. Furthermore, TF has been colocalized with VEGF in breast cancer, specially at sites of early angiogenesis. There are no data on the effect of hypoxia on tumor cell TF expression. Since hypoxia is known to stimulate VEGF production, we studied whether this also induces tumor cell TF expression. Confluent monolayers of A375 melanoma, MCF-7 breast carcinoma and A549 lung carcinoma were cultured in either 95% air, 5% CO2 (normoxic) or 95% N2, 5% CO2 (hypoxic; 25-30 mmHg) for 24 h. Procoagulant activity (PCA) was measured by amidolytic and clotting assays, surface TF antigen by flow cytometry, early apoptosis by annexin V binding and VEGF levels in Micardis Generic Cost culture supernatants by ELISA. Hypoxia significantly increased tumor cell PCA in all three cell lines tested and TF antigen on A375 cells was increased four-fold (P <0.05). Pentoxifylline (PTX), a methylxanthine derivative, significantly inhibited the hypoxia-induced increase in PCA as well as VEGF release in all three cell lines tested. In A375 cells, PTX significantly inhibited TF antigen expression by both normoxic and hypoxic cells. Hypoxia induced a slight (5%) but not significant, increase in early apoptosis. Intravenous injection of hypoxic A375 cells into nude rats produced more pronounced thrombocytopenia (n = 5, P <0.01) and more lung metastases (n = 3, P <0.05) compared to normoxic cells. We conclude that hypoxia increases TF expression by malignant cells which enhances tumor cell-platelet binding and hematogenous metastasis. Hypoxia-induced upregulation of TF appears to parallel that of VEGF, although the mechanism remains unclear.

trental brand name 2016-04-01

PTX administration 1 hour after induction of AP caused a Diovan Pills significant decrease in peritoneal levels of TNF-α and in serum levels of IL-6 and IL-10 when compared to the saline group. There were no differences in lung MPO activity between the two groups with AP. A decrease in mortality was observed in the PTX treatment compared to the saline group.

trental dosage dogs 2017-12-06

Neem oil, an extract of a native plant of India, has been demonstrated to have anti-fertility, anti-implantation, and abortifacient properties. An active fraction, termed NIM-76, was extracted that eliminates its abortifacient properties while retaining spermicidal activity. This fraction kills all human sperm in vitro in under 20 seconds at a concentration of 25 mg/ml. With increases in NIM-76 concentrations from 10 to 1000 mcg/ml, there was a linear decrease in percentages of motile as well as progressively motile sperm with time; also recorded were decreases in percentages of rapid, medium, and slow moving sperm, mean track speed, progressive velocity, mean linearity, and lateral head displacement and an increase in the percentage of static sperm. Electron microscopy revealed the formation of pores and vesicles over the sperm head, indicating damage to the cell membrane. Membrane fluidization studies did not reveal any significant change in the fluidity Cialis Low Dose of sperm cell membrane structure. Since calcium supplementation did not relieve the sperm from the spermicidal action, it was determined that NIM-76 does not cause any depletion of intracellular calcium. The capability of NIM-76 to selectively kill sperm without affecting normal cells makes it a highly desirable potential vaginal contraceptive agent.

trental drug class 2017-01-10

The development of new tuberculosis (TB) vaccines will require the identification of correlates of human protection. This study examined the balance between immunity and virulence in a whole blood infection model in which intracellular mycobacterial survival was measured using BACTEC. In the blood of tuberculin-negative donors, counts of Mycobacterium tuberculosis H(37)Ra organisms fell by 0.14 log(10) CFU during 96 h of whole Effexor 600 Mg blood culture, whereas counts of Mycobacterium bovis BCG, M. tuberculosis H(37)Rv, and a clinical TB isolate's organisms increased by 0.13, 0.43, and 1.04 log(10) CFU, respectively (P < 0.001), consistent with their relative virulence. Inhibition of tumor necrosis factor alpha by the addition of methylprednisolone or pentoxifylline or removal of CD4(+) or CD8(+) T cells by magnetic beads had deleterious effects on immune control of intracellular growth only in the blood of tuberculin-positive donors. Repeated vaccination of eight tuberculin-negative volunteers with M. bovis BCG resulted in a 0.3 log (50%) reduction in BCG CFU counts in the model compared to baseline values (P < 0.05). Three of the volunteers responded only after the second vaccination. These experiments indicate that whole blood culture may be used to measure immunity to M. tuberculosis and that further studies of repeated BCG vaccination are warranted.

trental 800 mg 2015-05-14

This randomized and blinded study was performed to determine whether pentoxifylline significantly improves tissue oxygenation after hemorrhagic shock. Hepatic surface oxygen tension was measured in anesthetized rats before and after hemorrhage. Rats were then randomly assigned to either a placebo group (n = 21) receiving 1 ml of intravenous saline solution or to a treatment group (n = 23) receiving intravenous 25 mg/kg of pentoxifylline in 1 ml of saline solution. Investigators were blinded as to which solution was injected. Five minutes after injection of pentoxifylline, there was significant increase in hepatic surface oxygen tension; this increase persisted throughout 1 hour of observation and was significantly Effexor Best Dose greater than in placebo-treated animals. Further study of the effects of pentoxifylline on tissue perfusion and oxygenation after hemorrhagic shock is warranted.

trental online buy 2017-11-23

In the present study altogether 51 patients with obliterating arteriosclerosis stage II according to Fontaine were examined concerning the haemodynamic and lipid parameters under influence of nifedipine and pentoxifylline, respectively. An antiatherogenic effect under nifedipine takes place possibly by the diminution of the triglycerides in the serum and the blood pressure as well as by the increase of the linolenic acid in the serum (precursor of the vasoprotective prostacyclin I3). Pentoxifylline essentially behaves lipid-neutral. The increase of the intermittent claudication distance clearly speaks for pentoxifylline. - Buy Levitra Reviews Nifedipine should only be used in concomitant indications.

online kopen trental 2017-01-16

Pentoxifylline significantly inhibited the in vitro proliferation of B16F10 cells in a concentration dependent manner and displayed an IC(50) of 15.2 mM. Non-cytotoxic concentration of 1-3 mM of PTX for an exposure of 24 h demonstrated significant changes in cell morphology. A significant inhibition in G1-S phase transition was observed on PTX treatment. Pretreated F10 cells showed inhibition in adhesion to ECM components and markedly inhibited the secretion of MMP-9 and MMP-2 Requip With Alcohol gelatinases.

trental 500 mg 2017-03-15

Randomised, placebo-controlled, parallel group trial. Patients with acute stroke were randomised within 24 h of stroke onset to IV therapy with placebo or Cerebrolysin 50 mL/day for 21 days. Both groups received concomitant treatment with ASA 250 mg/day Zyrtec Maximum Dosage PO and pentoxifylline 300 mg/day IV. Clinical examinations were performed on days 1, 3, 7, 21 and 90 post baseline. Outcome measures were the Canadian Neurological Scale, the Barthel Index, the Clinical Global Impressions, the Mini-Mental State Examination, and the Syndrome Short Test. Treatment emergent adverse events, lab tests, and vital signs were recorded to assess the safety of Cerebrolysin.

trental dosage 2016-02-11

Sixty-nine couples with previous failed IVF cycle, who had a low fertilization rate and/or male-factor infertility, were recruited to the study. Multiple follicular development was induced using the same protocol of human menopausal gonadotropin and gonadotropin releasing hormone analogue in both cycles. The oocytes were inseminated with spermatozoa treated with PF. The fertilization rates in the PF cycle were compared to the reference cycle based on semen analysis parameters and previous fertilization rates.

trental 400 mg 2015-11-14

Pentoxifylline, an effective membrane modifier, showed significant depletion in glutathione level in conjunction with increased lipid peroxidation. The results suggested an antimetastatic property by PTX at a nontoxic dose in B16F10 and B16F1 melanoma cells.

trental medication 2017-09-27

PTX attenuates both the decrease in airway patency and the increase in bronchial responsiveness induced by LPS inhalation, without any significant change in exhaled NO, which is increased by LPS inhalation.

trental y alcohol 2016-04-08

Cytokine-stimulated astrocytes and macrophages are potent producers of nitric oxide (NO), a free radical proposed to play an important role in organ-specific autoimmunity, including demyelinating diseases of the central nervous system. The aim of this study was to investigate effects of pentoxifylline (PTX), a phosphodiesterase inhibitor with immunomodulatory properties, on NO production and inducible NO synthase (iNOS) mRNA expression in rat astrocytes and macrophages. We have shown that PTX affects cytokine (interferon-gamma, IFN-gamma; interleukin-1, IL-1; tumour-necrosis factor-alpha, TNF-alpha)-induced NO production in both cell types, but in the opposite manner--enhancing in astrocytes and suppressive in macrophages. While PTX did not have any effect on enzymatic activity of iNOS in activated cells, expression of iNOS mRNA was elevated in astrocytes and decreased in macrophages treated with cytokines and PTX. Treatment with PTX alone affected neither NO production nor iNOS mRNA levels in astrocytes or macrophages. This study indicates involvement of different signalling pathways associated with iNOS induction in astrocytes and macrophages, thus emphasizing complexity of regulation of NO synthesis in different cell types.