No extensive studies were done that included the use of pentoxifylline or verify its effect on the outcome of ICSI in cases of mild and moderate asthenozoospermia.
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A rare case of simple ulcer of the colon in a 7-year-old girl is reported. Simple ulcer is clinically and pathologically recognized as a serious disease linked to intestinal Behcet's disease. Recently, some immunomodulators, such as thalidomide and antitumor necrosis factor monoclonal antibody, have been used to treat Behcet's disease, with varying degrees of success. Pentoxifylline (PTX) is also known to inhibit such inflammatory mediators as tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6. In this present patient combination treatment with prednisolone, azathioprine, and PTX improved corticosteroid dependence palliatively and prevented further relapse during a follow-up period of more than 12 months, without serious side effects.
The early phase of endotoxin-induced acute hemodynamic disturbances and hypoxemia is mediated by various factors, including eicosanoids and tumor necrosis factor-alpha (TNF alpha). Thromboxane A2 is the major mediator of the early pulmonary hypertension associated with endotoxemia, but the mechanisms underlying the prolonged hemodynamic disturbances observed in ongoing endotoxemia are not well understood. The authors used a chronically instrumental young piglet model to determine the roles of several eicosanoids and of TNF alpha in the prolonged endotoxin-induced pulmonary hypertension and other cardiovascular derangements. Animals were given 40 micrograms/kg endotoxin intravenously per hour for 30 minutes, followed by 20 micrograms/kg per hour. In all animals, persistent pulmonary hypertension, lowered cardiac output, any hypoxemia developed during endotoxin infusion. After 3 hours of endotoxin infusion, randomly ordered infusions of 1 mg/kg dazmegrel (a thromboxane A2 synthesis inhibitor), 5mg/kg nordihydroguaiaretic acid (a 5-lipoxygenase inhibitor), and 20 mg/kg pentoxifylline (A TNF alpha inhibitor) were given intravenously at 30-to-60-minute intervals. Dazmegrel and pentoxifylline lowered pulmonary arterial pressure and resistance and raised arterial oxygen tension. Cardiac output increased significantly after pentoxifylline. These hemodynamic effects persisted for 30-60 minutes, despite continued endotoxin infusion. The elevated plasma concentrations of thromboxane B2 and TNF alpha returned toward preendotoxin baseline values after dazmegrel and pentoxifylline treatment, respectively. No beneficial effects were noted after administration of nordihydroguaiaretic acid. Based on these results, both thromboxane A2 and TNF alpha, but not 5-lipoxygenase products, play active roles in prolonged endotoxin-induced pulmonary hypertension and hypoxemia in young piglets. Combined thromboxane A2 and TNF alpha blockade may be clinically useful in treatment of advanced sepsis in neonates.
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SACH impaired the motility and hyperactivation of rat sperm, which might result from the inhibition of GAPDS by SACH and subsequent defects of ATP and cAMP.
HIF-1α expression was higher in rabbits undergoing ESWL (group 4). In the hyperoxaluria group taking pentoxyphylline before ESWL (group 5), HIF-1α expression was lower in both early and late period subgroups (p < 0.05) CONCLUSION: In this study we evaluated HIF-1α expression and showed that ESWL may cause renal cell injury. Our results suggest that pentoxyphylline, as a circulatory regulator agent, may prevent renal cell injury induced by ESWL.
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PTX improved histological features of NASH compared to placebo. PTX was well tolerated in patients with NASH.
Thirty two patients who considered for selective nephrolithotomy were randomly assigned to 1 of 2 groups of 16 each; a single dose of IV PTX 500 mg bolus followed by IV infusion of PTX 700 mg for two hours or normal saline as placebo. Blood samples were obtained on the day before and the day after surgery and of C-reactive protein (CRP), creatine phosphokinase (CPK) and total antioxidant status (TAS) and catecholamines. Cortisol concentrations were also measured in 24-h urine samples.
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a review of the literature encompassing the pathogenesis of RR and the current therapeutic modalities available was performed.
Specific therapy for non-alcoholic steatohepatitis (NASH) is needed because of the potential severity of this liver disease. NASH is a recognized cause of cryptogenic cirrhosis and, increasingly, of hepatocellular carcinoma. Therefore, there is an unmet medical need for the therapy of NASH. This article discusses this therapy, with particular emphasis on pharmacologic therapy.
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PTX and Vit. E downregulated the expression of TGF-beta1 mRNA. The irradiated rat hearts showed a marked pathologic response to the drugs. The withdrawal of drugs in the 12th week postirradiation could cause rebound effects of the development of fibrosis.
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Alcoholic hepatitis is a clinical syndrome characterized by jaundice and liver impairment that occurs in patients with a history of heavy and prolonged alcohol use. The short-term mortality among patients with severe disease exceeds 30%. Prednisolone and pentoxifylline are both recommended for the treatment of severe alcoholic hepatitis, but uncertainty about their benefit persists.
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Flunarizine, a difluoro derivative of cinnarizine, produces a long-lasting inhibition of calcium-induced contractions of isolated vascular preparations of rabbit and rat. In this regard it is slightly more active than cinnarizine and markedly more active than papaverine, naftidrofuryl, bencyclane, cylandelate, dihydroergotoxine, xantinol nicotinate and pentoxifylline; calcium dobesilate does not inhibit the calcium-induced responses. A long-lasting antivasoconstrictor effect was observed also for cinnarizine. This action of flunarizine is selective for calcium channels in vascular tissue, since it has little effect on the calcium-induced response of myocardial preparations of the cat. Flunarizine has no effect on the rhythmic activity of myogenically active blood vessels; it thus shows a further selective activity to calcium channels activated by vasoconstrictor agents and not for those opened by intrinsic changes in membrane permeability. This dual selectivity implies that flunarizine is a useful reference substance in assessing calcium antagonism.
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Previous studies have demonstrated that one of the possible mechanisms responsible for the resistance of tumor cells to tumor necrosis factor-alpha (TNF-alpha) is the expression of TNF-alpha mRNA and/or protein. Pentoxifylline (PTX) suppressed TNF-alpha gene transcription and downregulates the expression of TNF-alpha mRNA and the secretion of TNF-alpha protein in macrophages and monocytes. This study investigates whether PTX downregulates the expression of TNF-alpha mRNA and/or protein in renal cell carcinoma (RCC) cells and whether PTX enhances the sensitivity of TNF-alpha-resistant RCC cells to TNF-alpha. Further, we explored whether PTX enhances the sensitivity of RCC cells to agents other than TNF-alpha by downregulation of the expression of TNF-alpha mRNA and protein. The R4 human RCC cell line constitutively expressed TNF-alpha mRNA and protein and was resistant to TNF-alpha. When R4 cells were incubated with PTX, the level of TNF-alpha mRNA and protein was markedly reduced. Pentoxifylline and TNF-alpha together overcame the resistance of R4 cells to TNF-alpha. The R11 human RCC cell line did not constitutively express TNF-alpha mRNA or protein, and was resistant to TNF-alpha. The expression of TNF-alpha mRNA in R11 cells, but not the production of TNF-alpha protein, was induced by TNF-alpha. When PTX was used in combination with TNF-alpha, the level of TNF-alpha mRNA induced by TNF-alpha was markedly reduced. The combination of PTX and TNF-alpha overcame the resistance of R11 cells to TNF-alpha. Pentoxifylline also enhanced the sensitivity of R4 cells to interferon-alpha. Pentoxifylline and anti-TNF-alpha monoclonal antibody augmented the sensitivity of R4 cells to cis-diamminedichloroplatinum (II) (CDDP). This study demonstrated that PTX, in combination with TNF-alpha, IFN-alpha or CDDP, overcame the drug resistance to RCC cells and that downregulation of TNF-alpha mRNA by PTX may be related to the cytotoxicity enhanced by the combination. The implications of these findings for clinical therapy are discussed.
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To investigate whether pentoxifylline could play a role in attenuation of the hazardous effects of ischemia/reperfusion on corporeal tissue in a rat model of veno-occlusive priapism (VOP).
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The decrease in TBARS levels and the increase in catalase activities suggest that normal hearts adapt compensatory mechanisms to prevent oxidative damage in response to the mild increase in SBP associated with WD. Use of PTX with WD further enhanced antioxidant activities probably to balance the potential increase in reactive oxygen species.
In 1987 and 1988 Nickisch et al. discussed the effect of infusions of prednisolone, pentoxifylline and, partially, piracetam in Ringer lactate solvent on progressive sensorineural hearing loss in childhood and adolescence. Time of observations was 4 years. Unfortunately long-term investigations could not confirm the initially good therapeutic results of 1987/88. In 35% were found permanently and in 12.5% temporarily better auditory thresholds after infusion. The loss of progressive sensorineural hearing in childhood usually takes a fateful course that can hardly be influenced. As is the case with adults, good therapeutic results can most probably be achieved by infusions starting close to the event, i.e. within 48 hours.
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To investigate the safety and efficacy of intravenous pentoxifylline infusion therapy, 600 mg twice daily for up to 21 days, for the management of patients with chronic critical limb ischaemia (CLI).
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Forty-five rabbits were divided into control group (C), electrical burn group (EB), and Pentoxifylline treatment group (PT) according to random number table, with 15 rabbits in each group. Model of HEB was reproduced in rabbits from EB and PT groups with voltage regulator and experimental transformer. Rabbits in C group were sham injured with the same devices without electrification. Changes in BCM were observed with microcirculation microscope at 15 minutes before HEB and 5 minutes, 1, 2, 4, 8 hour(s) post HEB (PHM or PHH), including: (1) morphology of microvessels, such as the discernible, diameters of arterioles, venules, and capillaries, the unevenness in caliber, and ischemic area; (2) dynamic changes in microvascular blood flow, such as blood flow speed in arterioles, venules, and capillaries, erythrocyte aggregation, and microthrombi formation; (3) condition of tissues surrounding microvessel, such as bleeding and exudation. Measurement data were processed with t test; enumeration data were processed with Fisher's exact test.
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To examine the protective effects of the vasodilator and hemorheologically active drug pentoxifylline and the calcium channel blocker nimodipine on the cochlea after acoustic overexposure in guinea pigs.
A simple and reliable method for the determination of pentoxifylline and its main metabolites in human plasma has been developed using high-performance liquid chromatography. After selective solid-phase extraction, pentoxifylline, its metabolites and an internal standard, 7-(2'-chloroethyl)theophylline, were separated on a 5-micron LiChrospher 100 RP-18 column using water-dioxan-acetonitrile (87:6.5:6.5, v/v/v) acidified with acetic acid (0.5%, v/v) as the mobile phase. The analytes were detected at 275 nm. The lowest detectable concentration for all analytes was 25 ng/ml; the recovery was 85%. The assay has been successfully applied to analysis of these compounds in human plasma after administration of an oral dose of 400 mg of pentoxifylline to healthy volunteers.
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The patholophysiologic significance of vascular congestion in the mechanism of ischemic acute renal failure following postocclusive reflow was studied with a novel hemorheologic probe, pentoxifylline. Using the autoperfused rat kidney model, inulin clearances (CIN), urine flow rates (UFR), renal electrolyte excretions, and renal hemodynamic parameters (RVR, RBP, RBF) were compared in saline- and pentoxifylline-treated anesthetized rats prior to and following a 45-min occlusive period. Renal functional and hemodynamic parameters were significantly altered in saline controls. In contrast, postischemia treatment with pentoxifylline was associated with significant recovery in CIN and UFR, and stable RVR, RBF, and RBP. Kidneys treated with saline infusion had pronounced vascular congestion, in contrast to those administered pentoxifylline. Coupled with the absence in medullary hyperemia, the present experiments support the role of vascular congestion in ischemic acute renal failure. Pentoxifylline, administered in pharmacologic doses after the insult, provided benefit during the initiation phase of postischemic acute renal failure. These data strengthen the opinion that ischemic insult results in vascular congestion, and that restoration of blood flow will prevent further deterioration in renal function.
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For human peritoneal mesothelial cell (HPMC) culture, a normal-glucose (NG, 5.5 mM) or HG (138 mM) medium was established through pilot experiments. The rat peritoneal dialysis (PD) model consists of four groups (n = 8): group 1, intraperitoneal (IP) HG (4.25%) solution; group 2, as group 1 plus daily IP PTX (4 mg/in 1 h); group 3, IP PTX and group 4 as control.