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)

The collapsed left lungs of dogs were subjected to 1 hour of normothermic ischemia in situ followed by immediate ligation of the contralateral pulmonary artery. Adenosine in a dose of 50 mg/kg prolonged the survival of the dogs significantly. In the survivors only transient changes in the chest x-ray were seen, and no changes in arterial oxygenation were observed. The pulmonary architecture was well preserved on histological studies 14 days after operation. Animals whose ischemic lungs were not protected by adenosine showed an immediate drop in arterial oxygenation and a massive infiltrate of the ischemic lung. Histological study of the lungs showed a complete breakdown of the capillary-alveolar barrier. Allopurinol alone was ineffective by itself and was not able to improve the survival achieved with adenosine further. We conclude that it is possible to prolong the tolerance of a deflated lung to normothermic ischemia by pretreatment with adenosine.
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PMID:The effect of adenosine and allopurinol on the tolerance of the collapsed lung to warm ischemia. 34 12

Allopurinol lowers peripheral vascular resistance in dogs, and it has beneficial effects upon muscular dystrophy patients. Since it has been suggested that muscular dystrophy may result from muscle ischemia, we decided to investigate the effects of allopurinol on skeletal muscle blood flow in normal and dystrophic mice. Arterioloar red cell velocity and diameters were measured in the cremaster muscle and used to calculate blood flow. Allopurinol (5 mg/kg, i.p.) resulted in an 81% increase in arteriolar blood flow in normal mice and a 102% increase in dystrophic mice. Such an increase in microcirculatory perfusion could be a mechanism contributing to the clinical effects of allopurinol.
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PMID:The effects of allopurinol on skeletal muscle microcirculation in normal and dystrophic mice. 52 75

Allopurinol, Collins' solution, and spermidine were tested for their ability to preserve nuclear function during kidney storage. Spermidine increased nuclear ribonucleic acid (RNA) polymerase activity 25 to 43 percent after 60 minutes of warm ischemia. Collins' solution was less effective and allopurinol did not protect RNA polymerase activity. Spermidine offered little additional protection over Collins' during cold storage of RNA polymerase activity. Only spermidine prevented the decrease in the molecular weight of RNA transcribed following kidney storage. Only Collins' solution prevented the breakdown of rapidly labeled heterogenous high molecular weight RNA and ribosomal precursor RNA.
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PMID:Protection of nuclear function by various agents during organ storage. 84 69

Ischemia and reperfusion of the small intestine and colon in rats were produced by reversible occlusion (for 30 min and 1 or 3 h) of the superior mesenteric artery and the aorta above the inferior mesenteric artery. Despite a greater reduction of mucosal perfusion in the colon than in the small intestine with 30 min of ischemia, the depth of mucosal damage was significantly smaller in the former than in the latter. Thirty minutes of ischemia followed by 1 h of reperfusion induced an increase in polymorphonuclear leukocyte infiltration in both locations. Exacerbation of mucosal injury occurred only in the small intestine, suggesting that reperfusion injury is independent of polymorphonuclear leukocyte infiltration. Reperfusion after 1 or 3 h of ischemia did not exacerbate mucosal damage in either location. Allopurinol significantly diminished the exacerbation of injury after reperfusion in the small intestine. The protective effect of allopurinol, however, was neither associated with an improvement in perfusion nor a reduction in polymorphonuclear leukocyte infiltration. These data indicate that there is a window (30 min) of reperfusion injury in the small intestine, but there is no evidence of reperfusion injury in the colon.
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PMID:Regional differences in gut blood flow and mucosal damage in response to ischemia and reperfusion. 141 42

Allopurinol and dimethyl sulfoxide (DMSO; 1 mL of 1, 2, or 5% by gavage daily) were used to examine the influence of scavenging oxygen-derived free radicals on the healing of reserpine- (5 mg/kg, intraperitoneal) and 5-hydroxytryptamine- (50 mg/kg, intraperitoneal) induced acute ischemic injury of the rat gastric mucosa. Allopurinol and DMSO demonstrated a time- but not dose-dependent power to stimulate healing of this injury. The magnitude of injury produced by reserpine or 5-hydroxytryptamine (serotonin) followed by gavage with allopurinol or DMSO was significantly (p < 0.01) less after day 4 than that after day 3 of this gavage, and the magnitude after day 3 was itself significantly (reserpine, p < 0.001; 5-hydroxytryptamine, p < 0.01) less than that after day 2 of the same gavage. The actions of allopurinol and DMSO were not associated with any significant influence on H+ output. These results suggest that oxygen-derived free radicals are detrimental to the integrity of the rat gastric mucosa and that scavenging them stimulates healing of the ischemia-induced injury of the mentioned mucosa.
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PMID:Stimulation of healing by free radical scavengers of ischemia-induced acute gastric mucosal injury in the rat. 144 12

To investigate the pathophysiology of warm ischemia (WI) of the liver, the changes in hemodynamics and energy metabolism were studied during and after 60-min complete WI induced by total hepatic vascular exclusion (HVE) in the canine model. Hepatic arterial blood flow after WI was maintained at 76% of the pre-ischemic level, while portal blood flow was only 27% of the pre-ischemic level associated with increased portal vein pressure, which was twice the pre-ischemic level, resulting in a decrease of total hepatic blood flow to 46% of the pre-ischemic level. Concentration of tissue lipid peroxide increased after WI. Arterial blood ketone body ratio (AKBR), which reflects the hepatic mitochondrial redox state, could not recover to the pre-ischemic level after termination of WI. However, when 100 mg/kg of allopurinol (xanthine oxidase inhibitor) was administered intravenously 10 min prior to initiating WI, AKBR was restored to the pre-ischemic level at 30 min after WI in spite of the fact that allopurinol administration to one group produced no remarkable changes in the hepatic hemodynamics compared with the group without allopurinol treatment. Concentration of adenine nucleotides was significantly higher for the treated group at the end of and after WI than for the group without allopurinol treatment and was maintained at a higher level even after WI. Lipid peroxide production was suppressed. Electron microscopic examination revealed that allopurinol treatment could not prevent mitochondrial swelling. It is suggested that WI causes injury primarily to the portal sinusoidal circulation, resulting in portal congestion concomitant with high portal pressure after the release of WI. Allopurinol could prevent the deterioration of mitochondrial ATP metabolism, and was able to inhibit lipid peroxide production, resulting in the rapid recovery of mitochondrial redox state in spite of the fact that it produced no amelioration of hepatic hemodynamics and morphological alterations.
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PMID:Preserved mitochondrial function by allopurinol despite deteriorated hemodynamics in warm ischemia-damaged canine liver. 148 Aug 16

We studied the effect of inhibition of oxyradical formation and of endogenous glutathione (GSH) depletion on lesion formation in the gastrointestinal tract in a modified rat hemorrhagic shock model (1 h hypotension and 1 h reperfusion). Allopurinol, an inhibitor of xanthine oxidase, did not protect against lesion formation. This suggests that oxygen radicals generated from xanthine oxidase may not be the major cause of injury under these conditions of prolonged 'ischemia'-reperfusion. Phorone (diisopropylideneacetone), a GSH depletor, decreased mucosal GSH levels in the corpus, duodenum and small intestine, and also significantly reduced lesion formation histologically in the corpus, antrum, duodenum and small intestine. However, there was no significant differences in mucosal blood flow (as estimated by changes in mucosal hemoglobin concentrations and oxygen saturation of mucosal hemoglobin) in the corpus, antrum, duodenum and small intestine between phorone-pretreated and control rats. We conclude that phorone decreased mucosal GSH concentrations and exerted a protective effect against hemorrhagic shock-induced gastrointestinal mucosal lesions. The protective effect appears to be independent of mucosal blood flow.
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PMID:Effect of phorone and allopurinol on ischemia-reperfusion injury in gastrointestinal mucosa of the rat. 150 63

Electrophysiological effects of allopurinol on arrhythmias were studied in isolated segments of guinea pig right ventricular free walls paced from endocardium. A high-gain electrocardiogram as well as transmembrane electrical activity from endo- and epicardium were recorded. Tissues were exposed to simulated ischemia for 15 min and then were reperfused with normal Tyrode solution. Sustained or nonsustained ventricular tachycardia, bigeminy, and trigeminy with characteristics of transmural reentry occurred in early reperfusion in 75% of 20 control preparations. Arrhythmias were associated with prolongation of transmural conduction time and abbreviation of endocardial effective refractory period (ERP). Allopurinol strongly reduced the incidence of reperfusion arrhythmias (20-33%) between 10 and 100 microM, whereas either lower or higher concentrations (5 or 500 microM) were less effective (43 and 50%). Antiarrhythmic efficacy correlated with significant attenuation of reperfusion-induced transmural conduction delay (P less than 0.05 or 0.01). Allopurinol did not affect endocardial conduction times nor did it significantly alter endocardial action potential duration or ERP. Our results indicate that allopurinol exerts antiarrhythmic efficacy during reperfusion by selectively attenuating defects related to anisotropic tissue properties.
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PMID:Effects of allopurinol on reperfusion arrhythmias in isolated ventricles. 151 Jan 30

Isolated working rat hearts were subjected to aerobic perfusion (25 min), cardioplegic infusion (3 min), global ischemia (30 min at 37 degrees C) and reperfusion (35 min). Measurements of myocardial xanthine oxidase and dehydrogenase activity, together with various adenine nucleotides and metabolites, were made at defined stages of the protocol (n = 6/group). Allopurinol pretreatment (20 mg/kg body wt/day for 3 days) improved the postischemic recovery of cardiac function; thus, aortic flow (a representative index) recovered to 68.8 +/- 4.2% compared with 53.2 +/- 2.3% in untreated controls (p less than 0.05). In fresh tissue, allopurinol pretreatment inhibited xanthine dehydrogenase activity by 73.1% (from 11.9 +/- 0.5 to 3.2 +/- 0.8 mIU/g wet wt: p less than 0.05) and xanthine oxidase activity by 95.2% (from 8.3 +/- 1.2 to 0.4 +/- 0.2 mIU/g wet wt: p less than 0.05); however, this inhibition was not maintained during perfusion. During reperfusion, myocardial xanthine dehydrogenase and oxidase activity was reduced by 40-60% (p less than 0.05) in both allopurinol pretreated and control hearts. Tissue content of creatine phosphate, adenosine triphosphate and catabolites, NAD and inorganic phosphate were not different in allopurinol pretreated or control hearts during either ischemia or reperfusion. This study does not support the concept that allopurinol protects the rat heart during ischemia and reperfusion by inhibition of xanthine oxidase activity or by conservation of purines. It appears that allopurinol achieves its protective effects by some, as yet undefined, mechanism.
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PMID:Allopurinol-enhanced myocardial protection does not involve xanthine oxidase inhibition or purine salvage. 152 Feb 48

Transient mucosal ischemia may cause oxygen-derived free radical production by xanthine oxidase, precipitating pouchitis after ileal pouch-anal anastomosis. Our aim, therefore, was to determine the effect of allopurinol, a xanthine oxidase inhibitor, in patients with acute and chronic pouchitis. Acute pouchitis was characterized clinically by sporadic episodes of increased frequency and decreased viscosity of stools, hematochezia, fever, malaise, and pelvic pain, which resolved promptly with treatment. Chronic pouchitis patients required continuous treatment to remain asymptomatic and invariably developed the signs and symptoms of pouchitis within one week following cessation of therapy. Eight patients with acute pouchitis were treated with allopurinol (300 mg p.o. b.i.d.) during the episode. Fourteen patients with chronic pouchitis had their standard antibiotic therapy discontinued while still asymptomatic; they were then given allopurinol (300 mg p.o. b.i.d.) for 28 days. Acute pouchitis resolved promptly in four of eight patients. Seven of the 14 patients with chronic pouchitis responded completely with no recurrence of symptoms during treatment. Allopurinol either terminated an episode of acute pouchitis or prevented pouchitis from recurring in 50 percent of patients. These data support a role for mucosal ischemia and oxygen free radical production in the etiology of pouchitis.
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PMID:Role of oxygen free radicals in the etiology of pouchitis. 156 95


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