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In 6 months old male Wistar rats 15 mg pentoxifylline/kg body weight were given intravenously in a single dose. The animals were sacrificed after 30, 60, 120 and 240 minutes respectively. It was confirmed that a single pentoxifylline administration enhanced prostacyclin generation by vascular and renal tissue samples, reaching its maximum 60 minutes after the treatment. The time course for PGI2-generation behaves differently in the tissues examined. It is concluded that the drug pentoxifylline might exert its beneficial role in the treatment of peripheral vascular disease at least in part by its influence on hemostatic balance at the endothelial-platelet interaction level.
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Ischemia/reperfusion injury can complicate recovery in cardiac operations. Ischemia induces endothelial dysfunction, which may contribute to leukocyte accumulation during reperfusion. Leukocyte-mediated injury may then occur. Using intravital microscopy we previously reported increased leukocyte retention in coronary capillaries and venules during early reperfusion during warm ischemia/reperfusion. In this study we investigated whether cold cardioplegic protection would limit leukocyte sequestration in coronary microvessels early in reperfusion. Pentoxifylline (PTX) has antiinflammatory effects and may limit endothelial dysfunction during ischemia/reperfusion. The effect of cardioplegia modification with PTX was also examined.
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Tibia fracture chronically up-regulated TNFalpha, IL-1beta and IL-6 mRNA and protein levels in hindpaw skin and PTX treatment significantly reduced the mRNA expression and cytokine protein levels for all these cytokines. PTX inhibited the nociceptive sensitization and some vascular changes, but had insignificant effects on most of the bone-related parameters measured in these studies. Immunostaining of hindpaw skin was negative for immunocyte infiltration at 4 weeks post-fracture.
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PTX was rapidly absorbed and eliminated after oral administration. Mean bioavailability after oral administration ranged from 15 to 32% among treatment groups and was not affected by the presence of food. Higher plasma PTX concentrations and apparent bioavailability were observed after oral administration of the first dose, compared with the last dose during the 5-day treatment regimens.
The hemorheological effect of KB-2796, 1-[bis(4-fluorophenyl)methyl]-4-(2,3,4,-trimethoxybenzyl)piperazine dihydrochloride, was studied in guinea pigs and rabbits in comparison with those of flunarizine (FNZ) and pentoxifylline (PXF). KB-2796 and FNZ at 10-100 microM dose-dependently prevented crenation of rabbit erythrocytes induced by the Ca2+ ionophore A23187. After incubation of guinea pig whole blood at 37 degrees C, blood micropore-filterability decreased and blood viscosity increased with the progress of erythrocyte crenation. After a 4-hr incubation, KB-2796 inhibited erythrocyte crenation and decreased blood filterability at a concentration of 30 microM, and it increased blood viscosity at 10 microM. Treatment with FNZ (30 microM) and PXF (100 microM) also inhibited erythrocyte crenation and decreased blood filterability. Intravenous administration of KB-2796 at 3 mg/kg significantly inhibited the decrease of blood micropore-filterability after occlusion of the bilateral carotid arteries in rabbits. Although FNZ (3 mg/kg, i.v.) had no effect, PXF (3 mg/kg, i.v.) produced significant inhibition. These results suggest that KB-2796 prevents increase of blood viscosity and decrease of blood filterability by inhibiting the crenation of erythrocytes and suggest that this effect may be useful for the improvement of hemorheology in ischemic disease.
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Individuals with HIV infection who were over 18 yr of age and free of opportunistic infections were recruited in the study and followed up 4 weekly. CD4 counts were measured using a flowcytometer using anti-human CD4 intervals. Pentoxiphylline was prescribed in a dose of 400 mg thrice daily.
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Oxidative stress is an important mechanism of contrast-induced acute kidney injury (CIAKI). The optimal strategy to prevent CIAKI remains unclear. The aim of the present study was to assess the effect of pentoxifylline, a nonspecific phosphodiesterase inhibitor, on the prevention of CIAKI. A total of 32 healthy male Sprague-Dawley rats were randomly divided into normal dietary group (NN; n=8) and a high cholesterol-supplemented dietary group (HN; 4% cholesterol and 1% cholic acid; n=24). At the end of eight weeks, the rats in the high cholesterol diet group were randomly divided into three subgroups (n=8 in each group). CIAKI was induced in two of the subgroups via intravenous injection of the radiocontrast media iohexol (10 ml/kg). Pentoxifylline (50 mg/kg) was administered to one of the iohexol-treated groups via intraperitoneal injection 12 h prior to and following contrast media (CM) injection. Kidney function parameters and oxidative stress markers were then measured. The renal pathological changes were evaluated using hematoxylin and eosin staining and scored semi-quantitatively. In iohexol-injected rats, serum creatinine (Scr), renal pathological scores, renal malondialdehyde (MDA) content, renal NADPH oxidase activity, fractional excretion of sodium (FENa%) and fractional excretion of potassium (FEK%) were significantly increased (P<0.01). The Scr, histologic scores, renal MDA content, NADPH oxidase activity, FENa% and FEK% in the rats treated with pentoxifylline prior to iohexol were observed to be reduced compared with those in rats treated with iohexol alone (P<0.01). This suggests that pentoxifylline significantly attenuates renal injuries, including tubular necrosis and proteinaceous casts induced by CM. It may be concluded that pentoxifylline protected the renal tissue from the nephrotoxicity induced by low-osmolar CM via an antioxidant effect.
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A chronic immune response involving proinflammatory T helper cell 1 (Th1) lymphocyte activation occurs in the atherosclerotic lesion, but whether this activation is protective or deleterious remains unclear. Methods and Results-- We modulated the immune response of the atherosclerosis-prone apolipoprotein E-deficient (apoE(-/-)) mouse. Eight-week-old apoE(-/-) mice were treated daily with pentoxifylline (PTX), a known inhibitor of the Th1 differentiation pathway, or PBS (control) for 4 weeks or 12 weeks. Twelve-week PTX treatment reduced atherosclerotic lesion size by 60% (P<0.01). PTX-treated mice developed lesions that were limited to the degree of fatty streaks. In contrast, control mice developed mature fibrofatty atherosclerotic lesions. In parallel, the proportion of interferon (IFN)-gamma-producing Th1 splenic lymphocytes was significantly reduced by PTX, and lesion size was correlated to the proportion of IFN-gamma(+) T cells. In vitro addition of PTX to cultured spleen cells did not modify the production of IFN-gamma but increased the production of IL-10 by T cells, indicating that PTX does not suppress IFN-gamma production but rather blocks Th1 polarization while promoting Th2 polarization.
Cilostazol, a novel oral phosphodiesterase inhibitor, has shown consistent improvement in exercise tolerance in patients with intermittent claudication (IC). In addition to this effect, cilostazol has previously been shown to have beneficial effects on the dyslipidemia, i.e., combination of high triglycerides with low high-density-lipoprotein cholesterol (HDL-C) levels. Interleukin-6 (IL-6) suppresses the activity of lipoprotein lipase, which modulates the metabolism of triglycerides and HDL-C. To determine whether a reduction of IL-6 contributes to the improvement of lipid profiles, we prospectively investigated the effect of cilostazol (n=16, 100 mg, twice daily) on the changes of lipid profiles and on the association with the changes of IL-6 compared with those of pentoxifylline (n=16, 400 mg, bid) in patients with IC. After eight weeks of administration of cilostazol to patients with IC, walking distances were increased, associated with a 29% decrease in plasma triglycerides and a 13% increase in HDL-C. No significant changes of lipid profiles in the pentoxifylline and placebo groups were observed although a similar improvement in walking distances was achieved in the pentoxifylline group. IL-6 levels were significantly reduced in patients receiving cilostazol as compared with those receiving placebo or pentoxifylline. The cilostazol-induced changes in the IL-6 were positively related to those of triglycerides in the cilostazol group (r=0.63, P<0.05) and negatively related to those of HDL-C (r=-0.55, P<0.05). These findings suggest that in addition to consistent improvement of exercise tolerance, cilostazol may improve lipid profiles by reducing IL-6 release. However, pentoxifylline did not affect lipid profiles although a similar improvement of maximal walking distance (MWD) was achieved.
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Bacterial intestinal infections is one of the most outstanding problems of international health service, preserving its significant clinical and social-economic importance. This group of infectious diseases is most frequently accompanied by the development of dehydration, thus leading to the development of nitrozative and oxidative stress. The presented data evidence the inhibiting action of pentoxifyllin for iNOS on dehydration, what may be manifested by decrease of severity of nitrozative and oxidative stress.
BAECs were cultured according to Schwartz's method, and one stage clotting time assay was used to measure TF activity.
Patients with human immunodeficiency virus (HIV) infection often suffer from persistent, painful ulcers that commonly occur on the soft palate, buccal mucosa, tonsillar area or tongue, which are referred to as aphthous ulcers. This paper reports the case in which pentoxifylline was successfully used to treat recurrent aphthous ulcers in an HIV patient.
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Preterm birth represents the single largest cause of mortality and morbidity for newborns and a major cause of morbidity for pregnant women. Tocolytic agents include a wide range of drugs that can inhibit labour to prolong pregnancy. This may gain time to allow the fetus to mature further before being born, permit antenatal corticosteroid administration for lung maturation, and allow time for intra-uterine transfer to a hospital with neonatal intensive care facilities. However, some tocolytic drugs are associated with severe side effects. Combinations of tocolytic drugs may be more effective over single tocolytic agents or no intervention, without adversely affecting the mother or neonate.
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Venous ulcers affect approximately 1% of the world's population, increasing healthcare expenditures and decreasing quality of life. Several hypotheses may help explain their origin. Incompetent veins or valves or impaired muscle function may lead to abnormal calf muscle pump function that can elevate ambulatory venous pressure (venous hypertension). This hypertension subsequently results in local venous dilatation and pooling, concomitantly trapping leukocytes that may release proteolytic enzymes that destroy tissues. Venous pooling also induces interendothelial pore widening and deposition of fibrin and other macromolecules that "trap" growth factors within them, rendering them unavailable for wound repair. Compression therapy, the mainstay treatment, reduces edema, reverses venous hypertension, and improves calf muscle pump function. Several treatment options can be employed as adjuvants to compression--eg, systemic therapy with pentoxifylline or aspirin, autologous grafts, tissue-engineered skin, growth factor therapy, and/or vein surgery. The epidemiology, pathophysiology, diagnosis, and management options regarding venous ulcers are reviewed.
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Pentoxifylline (PTF), a phosphodiesterase (PDE) inhibitor, can prevent inflammation and tissue damage in animal and in vitro human studies. However, the underlying mechanism remains unclear. Since Ca2+ is a critical signal regulating the release of inflammatory mediators in macrophages, the effects of PTF on Ca2+ influx were examined in NR8383 alveolar macrophages (AMs). PTF induced a dose-dependent inhibition on Ca2+ influx activated by zymosan and by protein kinase C (PKC) activators 1,2-dioctanoyl-sn-glycerol (DOG) or phorbol-12-myristate 13-acetate (PMA). The inhibition appeared to be specifically on the receptor-operated Ca2+ entry. The capacitative Ca2+ entry was not affected by PTF. The inhibition was not due to altered cAMP levels since the zymosan-activated Ca2+ influx was not affected by the adenylate cyclase activator forskolin, nor by dibutyryl cAMP. Pretreatment with protein tyrosine kinase (PTK) inhibitor genistein abolished zymosan-induced, but not DOG-induced Ca2+ influx, suggesting that PTK is an upstream element of the signaling cascade and not the target of PTF. The Ca2+ entry activated by zymosan and by PKC activators was inhibited by the mitogen-activated protein kinase (MAPK) inhibitor PD98059. Moreover, activation of MAPK by C6-ceramide (C6C) triggered a similar Ca2+ influx as elicited by zymosan and PKC activators, suggesting that MAPK is an element of the pathway. The C6C-induced Ca2+ influx was also inhibited by PTF. These results indicate that PTF blocks the receptor-operated Ca2+ influx in NR8383 AMs by inhibiting PDE which may acts as a downstream element of the signaling pathway or by direct interaction with Ca2+ channels.
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Similar to pentoxifylline, vinpocetine was also shown to have a beneficial effect over ischemic colon anastomoses.
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The results were comparable to those of previous studies, with positive responses seen in 63.6% of male patients and 61.5% of female patients. However, recurrence of ulcers was noted in all patients once the drug was discontinued. This was attributed to the small size of the patient sample studied and to the relatively short duration of treatment. No significant side effects were noted.
Aim of the study was to evaluate the efficacy, tolerance and safety of treatment of leg ulcer with pentoxiphylline administered orally in daily dose of 1200 mg divided for 3 doses for six months. The study was carried out in 19 centres in Poland. The results of clinical and laboratory (HGB, WBC, PTL) examinations made before, during and after treatment were documented in individual case-records. Pentoxiphylline was administered to 184 patients (124 F and 60 M) aged 22-86 (mean-61.6) yrs. One hundred and thirty-five patients had non-arterial ulcers, 37-partly arterial and 12-arterial. The duration of the disease was 1 to 1620 (mean 158) weeks. Resting pain was reported by 131 patients. In 9 persons the treatment was stopped after 1-2 months; in 6 (3%) of them due to side effects. In 175 patients pentoxiphylline was administered as follows: 1200 mg daily for 6 months in 92 cases, 1200 mg daily for 2-5 months--in 58, 1200 mg daily for 3-5 months and 800 mg daily for next 1-3 months--in 12 cases, and 800 mg daily for 1-6 months--in 13 cases. In 161 (92%) cases a beneficial effect was achieved including complete healing of the ulcers in 79 (45%) or improvement in 82 (47%); in 14 (8%) there was no improvement. The resting pain was significantly reduced in 114 (87%) patients within 1-24 weeks and completely disappeared in 69 (53%) patients within 2-20 weeks of treatment. No significant abnormalities in the results of laboratory tests were found. Transient side effects of the therapy appeared in 11 patients but they did not require administration of the drug to be discontinued. The study showed that pentoxiphylline is a effective, well tolerated and safe drug in the treatment of leg ulcers.
During the last decade, the cellular and plasmatic factors as well as fluid-dynamic conditions responsible for the 'anomalous' rheological behavior of blood have been clarified. Hypotheses about the hemodynamic significance of the hemorheological factors in microvascular perfusion can be formulated and have now been subjected to in vivo tests. Red cells have bipotential flow properties: as a consequence of passive, fluid-drop-like adaptation of RBC and membrane 'tank-treading' rapidly flowing mammalian blood has properties akin to an emulsion with extremely high fluidity - while slowly flowing blood becomes aggregated and assumes the properties of a concentrated reticulated suspension of low fluidity. In addition, in the normal microcirculation the fluidity of blood is maintained by rheological and vasomotor factors despite the fact that the cells are larger than the capillaries. Here, fluidity of blood flow thence critically depends a. on the presence of a minimum of shear forces sufficient to disperse aggregates and deform single cell, b. on the biochemical integrity of the vascular content which is prerequisite for normal RBC deformability, c. on the factors that keep microvascular hematocrit low. Under abnormal biophysical and/or biochemical conditions slowly flowing blood may suffer local loss of fluidity, under conditions of fluidity being abolished without coagulation. In hypoperfused microvascular beds, the variability of flow conditions, as well as the resulting variability of flow behavior is submitted as the cause of non-homogeneous perfusion ('collateral blood viscidation'). Hemorheological active drugs (such as pentoxifylline) cannot improve the deformability (fluidity) of normal erythrocytes, but they can protect the cells against the effect of rigidifying metabolites such as lactate, pH-drop, hyperosmolarity etc. Thus, they can maintain blood fluidity and thence residual flow despite abnormal flow behavior and flow conditions in hypoperfused organs. In vivo results corroborate the theory that factors which increase macroscopic blood viscosity in vitro are of small significance in the normal circulation (where they are likely to be compensated by vasodilatation). However, these same factors are critical to perfusion in the abnormal or decompensated circulation in the absence of adequate flow forces and following the recruitment of the limited vasodilator reserve of vital organs.
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An objective search for etiological bases should be conducted in any case of acute sensorineural hearing loss. The presence of cerebellopontine tumors in 7.5% of cases of SD, among other treated causes, justifies a thorough clinical investigation in these patients. Overall good evolution of hearing was observed in 67.5% of cases of SD, regardless of its etiology. Therapy within the first seven days of SD was significantly related to better outcomes in hearing.