Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There are several anecdotal reports of improvement in diabetic sensory neuropathy following a course of pentoxifylline therapy. Pentoxifylline theoretically could improve skin blood flow, thus reducing ischemia at axonal endings. The authors used laser Doppler techniques to measure skin blood flow and measured sine wave current perception thresholds (CPTs) in pentoxifylline-treated diabetic patients with sensory neuropathy. Twenty-four patients completed a six-month course of treatment. These patients had a predominantly "stocking" neuropathy; all the major abnormalities on clinical, laser Doppler, and current perception testing were found on the lower extremity. Seventeen of the 24 patients reported symptomatic improvement. A careful, graded neurologic examination confirmed that improvement, with a decrease in symptom score on the lower extremity (SSDW) from a baseline of 5.0 +/- 0.7 to 3.5 +/- 0.7 (p < 0.01) and of physical score (PSDW) from baseline 22.0 +/- 2.0 to 16.0 +/- 1.9 (p < 0.01) after six months. On the lower extremity, there was an increase in laser Doppler measured flow score (FS) both at 35 degrees and at 44 degrees C. FSDW (35 degrees) increased from 10 +/- 2 to 14 +/- 3 at six months (p < 0.05). FSDW (44 degrees) increased from 58 +/- 5 to 77 +/- 7 at six months (p < 0.01). There was an improvement in sine wave current perception measured by current perception threshold score (TS). TSDW dropped from 150 +/- 32 to 84 +/- 28 at six months (p < 0.03). In patients with diabetic sensory neuropathy, pentoxifylline appears to improve skin blood flow. Current perception thresholds improve in tandem, corroborating improvement in clinical neurologic findings.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Skin blood flow and current perception in pentoxifylline-treated diabetic neuropathy. 147 72

Pentoxifylline, a hemorheologic drug reputed to reduce blood viscosity, can be used to improve the microcirculation in peripheral vascular disease. The authors report on 2 patients who were being followed up for possible glaucoma and whose visual field constriction became worse at about the same time as their peripheral vascular symptoms began to increase in severity. Following initiation of treatment with oral pentoxifylline, their peripheral vascular complaints decreased and their visual fields gradually expanded over the next several months. This dual effect seemed more than a coincidence. It may in fact indicate that the same mechanism said to aggravate the peripheral ischemia (ie, increased blood viscosity) in patients with peripheral vascular disease may also have been the basis for the visual field contraction in these 2 patients, possibly by producing retinal ischemia. The reversal of the contracted visual fields would then seem to be due to the ameliorative effect of the pentoxifylline treatment on the blood viscosity.
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PMID:Expansion of contracted visual fields following treatment with pentoxifylline in two patients with coexistent peripheral vascular disease--case reports. 155 23

Painful diabetic distal sensory neuropathy is a disabling and common complication of diabetes mellitus. There is evidence that microvascular changes resulting in ischemia to the vasa nervorum may contribute to this problem. Pentoxifylline has been shown to improve circulation through partially occluded peripheral vessels and has been postulated to be of potential benefit. Forty adult type II diabetics were enrolled in a double-blind, placebo-controlled study utilizing pentoxifylline for six months. Visual analog scores, nerve conduction studies, and physical examinations were used to evaluate response to treatment. At the end of the six-month trial, there was no significant difference in the patients' pain between the pentoxifylline- and placebo-treated groups. The authors conclude that pentoxifylline is not useful in the treatment of painful distal diabetic neuropathy.
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PMID:Pentoxifylline in the treatment of distal diabetic neuropathy. 192 15

In this article a new model of peripheral occlusive arterial disease is described. The lower hindlimb of an anesthetized ferret was fixed to a holder, the distal end of the Achilles tendon attached to an isometric force transducer, and a passive preload of 100 g was applied to the muscle preparation. The hindlimb was stimulated to contract isometrically via supramaximal electrical stimulation of the sciatic nerve. During the initial period, when femoral blood pressure equaled aortic blood pressure, net contractile force peaked within 1 or 2 min (372 +/- 24g, n = 20) and gradually declined to about 85% of peak over 20 min. Following 60 min of ischemia (induced by partial occlusion of the abdominal aorta), when blood pressure in the contralateral femoral artery was about 45 mm Hg, the 15-min area under the force-time curve (AUC) was 33.2 +/- 2.5% (n = 4) of the initial value. To validate the utility of this model in the search for treatment of peripheral vascular diseases, two drugs were tested. Pentoxifylline, which is clinically effective, attenuated the loss of function observed during ischemia in a dose-related manner, but nifedipine, which is without clinical benefit, had no effect at a dose that was extremely hypotensive. Because femoral perfusion pressure was controlled, systemic hemodynamic effects of test compounds are minimized as potential mechanisms of action, simplifying the evaluation of novel pharmacotherapy for treatment of ischemic diseases.
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PMID:Drug effects on function in the ferret ischemic hindlimb. 237 Aug 4

Random skin flaps are an important and frequently used technique in head and neck reconstruction. Pentoxifylline has been shown to improve the deformability of red blood cells by increasing their intracellular adenosine triphosphate content and, therefore, improving their flow properties. This is especially important in ischemia and low blood flow states present in the distal portions of random skin flaps. The rheologic properties of pentoxifylline were studied in the swine model. Swine in group I (eight flaps) served as controls with no pharmacologic manipulations. Swine in group II (16 flaps) received pentoxifylline (20 mg/kg/d) for ten days preoperatively and ten days postoperatively. Necrosis in swine in group I (controls) averaged 32.6%, which substantiated previous reports. Necrosis in swine in group II (pentoxifylline) averaged 2.57%. This study has shown a statistically significant enhancement of random skin flap survival using pentoxifylline in a swine model.
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PMID:The effects of pentoxifylline on random skin flap survival. 291 88

Pentoxifylline 0.3--30 mg/kg was given intravenously to six dogs under nitrous oxide anesthesia. Cerebral blood flow was measured with a sagittal sinus outflow technique, cerebral oxygen consumption was calculated from the a-v difference, and metabolite levels were determined in biopsies of cerebral cortex. Pentoxifylline failed to influence cerebral blood flow or oxygen consumption. There was no increase in cerebral levels of phosphocreatine, ATP or total adenine nucleotides; the only significant effect was higher glucose levels in dogs given pentoxifylline (4.49 +/- 0.39 mumol/g vs 2.21 +/- 0.18 mumol/g). The latter has previously been reported to be deleterious during cerebral ischemia. Pentoxifylline thus failed to have any significant influence upon cerebral blood flow or metabolism in the dog likely to be of benefit during cerebral hypoxia or ischemia.
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PMID:Pentoxifylline does not change cerebral blood flow or metabolism in the dog. 679 17

The effect of pretreatment with pentoxifylline on normothermic liver ischemia was studied in rats. This drug, a dimethylxanthine and fosfodiesterase inhibitor, improves microcirculation, decreases neutrophil activity in experimental sepsis and hemorrhagic shock, and inhibits "in vitro" cytokine production by isolated Kupffer cells. Partial liver ischemia was induced by occlusion of afferent vessels to the median and left lateral lobes for 60', followed by resection of nonischemic lobes just before reperfusion. The rats were divided in 4 groups: I (n = 6) sham operation, II (n = 6) resection of right and caudate lobes, III (n = 42) normal saline pretreatment and 60' ischemia, IV (n = 42) pentoxyfilline pretreatment (50mg/K/i.p. 2 h before clamping) and 60' ischemia. 12 animals were sacrificed 1 h and 6 h after reperfusion respectively (gr III and IV), and 20 rats were observed for a maximum of 24 h after reperfusion. Serum transaminases, LDH, CK (isoenzymes), bilirubin, and total bile acids were determined in each animal. A sample of the left lobe was taken for histological examination. Extent of necrosis 24 h after reperfusion was assessed. Bile output was measured before ischemia and during the first hour of reperfusion. Pentoxifylline pretreatment was associated with a lower rise in serum transaminases and LDH after reperfusion, but it did not modify the changes in either serum CK activity (mainly CKBB), or total bile acid concentration. A reduction of bile output was not avoided by pentoxifylline pretreatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Liver damage due to normothermic ischemia and reperfusion in the rat. The effects of pentoxifylline pretreatment]. 766 19

This study examines the hypothesis that pentoxifylline protects renal PGE2 synthesis during mesenteric ischemia/reperfusion injury. Anesthetized Sprague-Dawley rats (300 g) were subjected to sham or superior mesenteric artery occlusion for 20 min followed by 30 min of reperfusion. The ischemia/reperfusion groups received either enteral allopurinol (10 mg/kg) daily for 5 d prior to ischemia, pentoxifylline (50 mg/kg) 10 min prior to ischemia or carrier. The kidney was removed and perfused in vitro with oxygenated Krebs buffer and the effluent was assayed for release of 6-keto-PGF1 alpha, PGE2 and thromboxane B2 (TXB2) by enzyme immunoassay. Mesenteric ischemia/reperfusion decreased renal PGE2 release by 50% (compared to sham) but did not alter release of TXB2 or 6-keto-PGF1 alpha. Pentoxifylline pretreatment (not allopurinol) preserved renal PGE2 release at the sham level. These data showed pentoxifylline exerted a protective effect against severe mesenteric ischemia/reperfusion injury by maintaining release of renal PGE2, a potent endogenous renal vasodilator.
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PMID:Acute mesenteric ischemia/reperfusion down regulates renal PGE2 synthesis. 770 19

Inhibition of pulmonary neutrophil sequestration attenuates ischemia-reperfusion (IR) lung injury. Pentoxifylline (PTX) reduced pulmonary sequestration of neutrophils and neutrophil-dependent lung injury in several experimental settings but has never been tested in IR models. We hypothesized that PTX may have a beneficial effect on IR lung injury as measured by the coefficient of filtration (Kfc) and may reduce IR-associated sequestration of neutrophils as assessed by lung myeloperoxidase (MPO) activity and by blood neutrophil count decrease during reperfusion. Three groups of isolated blood perfused rat lungs were studied: a time control group (n = 6) was perfused for 3 h, and two groups (n = 10) subjected to 1 h ischemia were treated with PTX or saline before a 2 h reperfusion. The increase in Kfc induced by IR was reduced fivefold by PTX compared with saline (+27 +/- 8% versus +112 +/- 12%, respectively; p < 0.001), and was similar to time controls (+9 +/- 9%). After IR, MPO and blood neutrophil count decrease were lower with PTX than with saline. Changes in Kfc were correlated to the percentage decrease in blood neutrophils during reperfusion. We conclude that PTX reduced rat lung IR microvascular injury. This effect may be mainly caused by decrease in lung sequestration of neutrophils during reperfusion.
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PMID:Reduction of ischemia-reperfusion injury by pentoxifylline in the isolated rat lung. Paris-Sud University Lung Transplantation Group. 804 13

The authors studied the effects of a combination of pentoxifylline and nimodipine on cerebral lipid peroxidation in postischemic rat brain. Pentoxifylline (40 mg/kg) and nimodipine (3 mg/kg) were administered per os 30 min before 5 min of ischemia (four-vessel occlusion model of transient ischemia). The extent of peroxidation in brain tissue (cerebral cortex, hippocampus, striatum) was then estimated by assay of thiobarbituric acid reactive substances (TBARS). The concentration of TBARS was significantly lower in the cerebral cortex and hippocampus of the group treated with the combination of drugs than in untreated ischemic rats. However, this concentration was not significantly different from that found in the cerebral cortex and hippocampus of other groups premedicated with nimodipine or pentoxifylline alone. The tested drugs had no effect on TBARS in the striatum. The hypothesis that the combination of drugs would have a synergistic effect on postischemic lipid peroxidation was therefore not confirmed.
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PMID:Effect of a combination of pentoxifylline and nimodipine on lipid peroxidation in postischemic rat brain. 853 30


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