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Treatment of idiopathic peripheral facial paralysis has remained controversial in many aspects. The authors report their experience with a protocol based on high-dose prednisolone with intravenous low-molecular-weight dextran and pentoxifylline. For this regimen, the term antiphlogistic-rheologic infusion therapy (ARIT) has been coined.
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Pentoxifylline, a dimethyl xanthine derivative given to patients with peripheral vascular disorders, increases erythrocyte deformability, diminishes Ca2+ entry, inhibits Ca(2+)-dependent transglutaminase activity and elevates ATP levels. The present study examined the effects of pentoxifylline on the Ca2+ pump ATPase, an enzyme which regulates intracellular Ca2+ levels. Studies were carried out with inside-out vesicles (IOVs) prepared from young (Ey) and old (Eo) human and rat erythrocytes. The pumping of Ca2+ depends on the concomitant hydrolysis of ATP; the two processes were measured using radiolabeled substrates. The catalytic properties of IOVs from young and old erythrocytes were stimulated by pentoxifylline when added directly to the assay medium. Pentoxifylline (0.5 to 5.0 mM) significantly activated the rates of Ca2+ dependent ATP hydrolysis in Ey and Eo IOVs of rat erythrocytes. The percent of activation was greater in the IOVs from older erythrocytes. The Ca2+ translocation was also affected by pentoxifylline. The early burst of Ca2+ uptake into IOVs decreased in the presence of pentoxifylline in Ey IOVs prepared from either species whereas steady state rates of Ca2+ transport only declined at 5.0 mM pentoxifylline. This pattern was not evident in the corresponding Eo IOVs. The response of Ey and Eo IOVs to pentoxifylline may be the basis of the difference in sensitivity of young and old erythrocytes to the drug in regulating intracellular Ca2+ concentrations.
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The purpose of this study was to assess the prophylactic effect of pentoxifylline (Ptx) on complications related to radiation.
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This study investigated the effects of pre- and post-laparoscopic conditioning, zinc, pentoxifylline (PTX), and N-acetylcysteine (NAC) on markers of I/R injury in an animal model.
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The findings demonstrate that the efficacy of the pentoxifylline is not statistically equivalent to the efficacy of prednisolone, supporting the use of prednisolone as a preferred treatment option in patients with severe alcoholic hepatitis.
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Six control dogs received pentoxifylline (40 mg/kg bolus followed by infusion at 0.2 mg/kg/hr) without ischemia. Thirteen dogs received Ringer's lactate solution with 12 mins of cerebral global ischemia (by aortic occlusion). Nine dogs received pentoxifylline before ischemic insult. Six dogs received pentoxifylline on reperfusion, and six dogs received pentoxifylline 30 mins after reperfusion.
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Twenty-two trials met the inclusion criteria involving a total of 1200 participants with stable leg pain. Follow-up period was from two weeks to two years. There was some variation in the exercise regimens used, all recommended at least two sessions weekly of mostly supervised exercise. All trials used a treadmill walking test for one of the outcome measures. Quality of the included trials was good, though the majority of trials were small with 20 to 49 participants. Fourteen trials compared exercise with usual care or placebo; patients with various medical conditions or other pre-existing limitations to their exercise capacity were generally excluded.Compared with usual care or placebo, exercise significantly improved maximal walking time: mean difference (MD) 5.12 minutes (95% confidence interval (CI) 4.51 to 5.72;) with an overall improvement in walking ability of approximately 50% to 200%; exercise did not affect the ankle brachial pressure index (ABPI) (MD -0.01, 95% CI -0.05 to 0.04). Walking distances were also significantly improved: pain-free walking distance MD 82.19 metres (95% CI 71.73 to 92.65) and maximum walking distance MD 113.20 metres (95% CI 94.96 to 131.43). Improvements were seen for up to two years. The effect of exercise compared with placebo or usual care was inconclusive on mortality, amputation and peak exercise calf blood flow due to limited data.Evidence was generally limited for exercise compared with surgical intervention, angioplasty, antiplatelet therapy, pentoxifylline, iloprost and pneumatic foot and calf compression due to small numbers of trials and participants. Angioplasty may produce greater improvements than exercise in the short term but this effect may not be sustained.
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Reactive oxygen species (ROS), particularly hydroxyl radical (HO*), increase neutrophil adherence to hypoxanthine-xanthine oxidase (HX-XO)-treated human umbilical vein endothelial cells (HUVEC) in culture. This adherence is inhibited by the tyrosine kinase inhibitors genistein (30 microM) and herbimycin A (0.9 microM), suggesting the involvement of tyrosine kinase. Phosphorylation of several HUVEC proteins in the range of 120-130 and 70 kDa was found to depend on the XO concentration and stimulation time. This phosphorylation was inhibited by the antioxidants dimethylthiourea (DMTU, 0.75 to 7.5 mM) and pentoxifylline (Ptx, 0.1 mM), and by the iron chelators desferrioxamine (DF, 1 mM) and hydroxybenzyl ethylene diamine (HBED, 0.5 mM), suggesting the involvement of HO*. Three tyrosine-phosphorylated proteins, focal adhesion kinase (p125FAK), paxillin (PAX) and p130cas were isolated and characterized by immunoprecipitation and western blotting. Antioxidants and iron chelators reduced their phosphorylation. HUVEC treated with ROS for 15 min showed actin stress fiber formation. Cytochalasin D (5 microM) inhibited tyrosine phosphorylation and PMN-HUVEC adherence, showing the importance of cytoskeleton integrity in these two functions. In conclusion, HO*, which is involved in increased PMN-HUVEC adhesion, also increases tyrosine phosphorylation on three major cytoskeleton proteins which seem to play a role in this adhesion.
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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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Epidural fibrosis (EF) is a major cause of failed back surgery syndrome (FBSS), which induces disabling radiculopathy for which no effective medical treatment exists. Our understanding of the fibrosis mechanisms and our clinical and experimental results for the treatment of radiation-induced fibrosis prompted us to postulate that EF might respond to treatment with combined pentoxifylline (PTX)-tocopherol (Vit.E). 6 weeks after lumbar spine surgery, a 28-year-old man presented with recurrent left L5 sciatica without disc herniation on MRI in December 1993. From 1993 to 1997, he had unrelieved back and leg pain, which became increasingly resistant to intensive medical treatment and to a spinal cord stimulator, and confined him to bed as from December 1997. In 1998, a lumbar CT-scan showed an area of left L4-L5 EF measuring 12 mm x 12 mm, without disc herniation. From April 1998, oral PTX (800 mg day(-1)) and Vit.E (1000 IU day(-1)) were administered daily for 3.5 years and well tolerated. Clinical improvement began during the third month of treatment and continued until total regression of clinical symptoms April 2001. Lumbar MRI in November 2001 showed a surface area of residual EF half the size of the initial area. This is the first report to indicate that antifibrotic treatment using combined PTX-Vit.E may be of potential benefit in the treatment of post-operative EF. Additional studies are required to confirm this potential.
Following the induction of CAIA, mice developed transient joint inflammation. In contrast, pain-like behavior was observed prior to, and outlasted, the visual signs of arthritis. Whereas gabapentin and buprenorphine attenuated mechanical hypersensitivity during both the inflammatory and postinflammatory phases of arthritis, diclofenac was antinociceptive only during the inflammatory phase. Spinal astrocytes and microglia displayed time-dependent signs of activation, and inhibition of glial activity reversed CAIA-induced mechanical hypersensitivity.
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On the seventh day, percentage of the necrotic area was significantly reduced in PTX, HLD, and PTX-HLD animals compared with control groups. On 14th day, percentage of the necrotic area in PTX, HDL, and PTX-HLD groups was also significantly reduced compared with control groups. PTX and PTX-HLD showed a significant reduction in dermis cellularity, VV of macrophages, and myofibroblasts compared with control groups; PTX showed a significant enhancement of LV of blood vessels compared with all other groups.
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The ability of two supposed DNA-repair inhibitors to modulate cisplatin-induced cytotoxicity in a human ovarian cancer cell line (CAOV-3) and a human cervical cancer cell line (Me-180) was investigated using a short-term chemosensitivity assay based on bioluminescence of cellular adenosine triphosphate (ATP). Cisplatin concentrations bracketing the reported peak plasma concentration (2.5 micrograms/ml) were used and the 50% inhibitory concentrations were determined by linear regression of log-transformed survival data. At 2.5 mM, the methylxanthine caffeine enhanced cisplatin sensitivity 2.9-fold in CAOV-3 cells and 2.7-fold in Me-180 cells. At 2.5 mM, pentoxifylline, a closely related methylxanthine, increased cisplatin sensitivity 2.9-fold in CAOV-3 cells and 3.4-fold in Me-180 cells. Chemical modification of cisplatin-induced cytotoxicity by assumed inhibition of DNA-repair mechanisms may hold promise for clinical application in the treatment of gynecological cancer.
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Pentoxifylline administration prevented excessive weight gain but did not affect hyperinsulinemia or hypertriglyceridemia seen in metabolic syndrome animals. In addition, pentoxifylline prevented the elevations in mean blood pressure associated with metabolic syndrome. Particularly, pentoxifylline prevented elevations in systolic, diastolic, and notch blood pressure; however, elevation in pulse blood pressure was not affected. Further, pentoxifylline alleviated the low-grade inflammation associated with metabolic syndrome, as reflected by the significantly lower serum tumor necrosis factor α and higher serum adiponectin levels metabolic syndrome animals treated with pentoxifylline. Also, pentoxifylline inhibited elevated expression of angiotensin receptor 1 in aortic tissue of metabolic syndrome animals.
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Among the factors involved in the early complications of lung transplantation is the ischemia-reperfusion syndrome related to a warm reperfusion in ischemic lungs.
Prospective, randomized, and blinded survival studies were performed with two lisofylline dosing regimens added to fluid resuscitation in a shock model. In addition, white cell adhesiveness was measured to assess the effects of lisofylline.
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We assessed the safety and efficacy of intravenous pentoxifylline [3,7-dimethyl-1-(5-oxohexyl)-xanthine] in patients at risk for developing multiple organ failure after major cardio-thoracic surgery in a single-center, randomized, placebo-controlled study. Of 816 consecutive patients who underwent major cardio-thoracic surgery, 40 who had Acute Physiology and Chronic Health Evaluation II score values > or = 19 at the first postoperative day after the surgery were included. Patients were randomized to receive either placebo (control; n = 25) or intravenous pentoxifylline treatment (pentoxifylline; n = 15) at a dosage of 1.5 mg/kg/h as an adjunct to standard supportive therapy. Main outcome measurements were duration of required ventilator support, intensive care unit stay, and incidence of renal failure. Thirty-seven patients were eligible for evaluation. No significant adverse events related to pentoxifylline treatment were observed. The duration of mechanical ventilation was significantly greater for control patients (8.3 +/- 3.1 days) compared with pentoxifylline-treated patients (3.1 +/- .9 days; p < .05). Patients treated with pentoxifylline experienced fewer days on hemofiltration (1.2 +/- .8 vs. 6.8 +/- 3.3; p < .05) and a shorter intensive care unit stay (5.2 +/- 1.1 vs. 11.4 +/- 3.1 days). There were no intergroup differences in mortality. Mortality was 33% in the pentoxifylline group and 36% among control group patients. In conclusion, supplemental pentoxifylline treatment may decrease the incidence of multiple organ failure in patients at risk of systemic inflammatory response syndrome after cardiac surgery. Additional studies are required to determine the validity of the observed effects.
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Until the mid-1990s, radiation-induced normal-tissue injury was generally assumed to be solely caused by the delayed mitotic death of parenchymal or vascular cells, and these injuries were held to be progressive and untreatable. From this assumption, it followed that postirradiation interventions would be unlikely to reduce either the incidence or the severity of radiation-induced normal tissue injury. It is now clear that parenchymal and vascular cells are active participants in the response to radiation injury, an observation that allows for the possibility of pharmacologic mitigation and/or treatment of these injuries. Mitigation or treatment of chronic radiation injuries has now been experimentally shown in multiple organ systems (eg, lung, kidney, and brain), with different pharmacologic agents (eg, angiotensin-converting enzyme inhibitors, pentoxifylline, and superoxide dismutase mimetics) and with seemingly different mechanisms (eg, suppression of the renin-angiotensin system and suppression of chronic oxidative stress). Unfortunately, the mechanistic basis for most of the experimental successes has not been established, and assessment of the utility of these agents for clinical use has been slow. Clinical development of pharmacologic approaches to mitigation or treatment of chronic radiation injuries could lead to significant improvement in survival and quality of life for radiotherapy patients and for victims of radiation accidents or nuclear terrorism.
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Pentoxifylline is a xanthine derivative with hemorrheologic and vascular properties that may improve gas exchange in patients with chronic obstructive pulmonary disease (COPD). We tested this hypothesis in 12 patients with COPD (mean FEV1 = 40 percent predicted; mean DCO, 8.6 ml/min/mm Hg) randomly divided into a treatment and control group and six healthy volunteers. Following establishment of baseline DCO and maximum expiratory flow volume (MEFV) curve values, each subject in the treatment and healthy groups took 400 mg of pentoxifylline three times a day for 12 weeks. Weekly DCO and MEFV curves were measured before treadmill exercise in both COPD groups and before and after exercise in the healthy group. The MEFV curve parameters from the final three weeks of therapy did not differ significantly from baseline values. During this time, however, the treatment COPD group's resting DCO rose by 8.2 +/- 2.4 percent over baseline level (p less than 0.01). Treadmill walk time increased from 17.7 +/- 2.9 minutes to 23.2 +/- 2.9 minutes (p less than 0.02). This was accompanied by improved exercise oxygen saturation measured by oximetry (SoxiO2). Premedication SoxiO2 fell from 92.8 +/- 1.2 percent to 88.6 +/- 2.5 percent during exercise, and from 94.4 +/- 1.1 percent to only 91.8 +/- 1.0 percent after 12 weeks of medication (p less than 0.05). No such improvement was noted in the control COPD group. Although the healthy group's resting SoxiO2 and DCO did not change during treatment, their exercise DCO increased significantly from 36.3 +/- 3.1 ml/min/mm Hg to 41.8 +/- 3.5 ml/min/mm Hg (p less than 0.001). These data demonstrate that pentoxifylline improves gas exchange, possibly by increasing cardiac output, and/or by raising mixed venous PO2, and/or by improving blood flow to underperfused alveoli.
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There is some evidence of benefit for thalidomide and clofazimine, but generally we did not find clear benefits for interventions in the management of ENL. This does not mean they do not work because the studies were small and poorly reported. Larger studies using clear definitions and internationally recognised scales are urgently required.
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This study shows that a novel route (via the pulmonary circulation) used to administer pentoxifylline after hemorrhagic shock leads to superior cardiac performance in comparison with administration via lactated Ringer's solution or i.v. systemic pentoxifylline.
The distal tibia was fractured and the hindlimb casted for 4 weeks. The rats were given drinking water with or without the cytokine inhibitor pentoxifylline (PTX) starting the day before fracture and continuing for 4 weeks, after which time the cast was removed and multiple assays were performed in the hindpaw. PCR and immunoassays were used to evaluate changes in cytokine expression. Bilateral hindpaw thickness, temperature, and nociceptive thresholds were determined, and bone microarchitecture was measured by microcomputed tomography (microCT).