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)

SC-29333 (SC) has been reported to protect the gastric mucosa from the effects of topical aspirin. We compared SC and 16,16-dimethyl PGE2 (16-dm) in 20 chambered canine stomachs (6 controls and 7 of each PG). Prostaglandin was added to an acid solution (100 mM HCl; 54 mM NaCl) at 0, .001, .01, 0.1, and 1.0 microgram/ml (two periods each). Then aspirin (20 mM) and PG (1.0 microgram/ml) (two periods) were followed by hemorrhagic shock (near 60 mm Hg mean arterial pressure). 16-dm caused a significant efflux of fluid (-6.5 +/- 5.3 to 17.3 +/- 6.7 microliters/min), Na+ (2.1 +/- 0.5 to 6.8 +/- 1.6 muEq/min), and Cl- (-0.9 +/- 2.4 to 5.3 +/- 1.3 muEq/min), but did not affect K+ or H+. 16-dm also caused a slight drop in potential difference (PD) (67.6 +/- 1.7 to 60.3 +/- 2.0 mV). 16-dm did not significantly affect total blood flow. Percent lesion formation was more severe than controls (20.2 +/- 3.5 vs 11.6 +/- 1.7 percent) but not statistically significant. SC had no significant effect on fluid, H+, Na+, K+, or Cl-. It caused an increase in blood flow (6.85 +/- 1.46 to 26.20 +/- 2.74 ml/min, p less than .001). SC significantly reduced percent lesion formation (1.9 +/- 0.9% p less than .001). We conclude: 1) SC causes an increase in mucosal blood flow and protects from aspirin-shock ulcerogenesis. 2) 16-dm stimulates an efflux of non-parietal extracellular fluid and fails to protect against aspirin injury during mucosal ischemia. 3) SC cytoprotection may be mediated by increased mucosal blood flow. 4) The mechanism of cytoprotection with 16-dm may require sufficient mucosal blood flow for filtration of non-acid fluid from blood to gastric lumen.
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PMID:The cytoprotective effects of (+/-)-15-deoxy-16-alpha, beta-hydroxy-16-methyl PGE1 methyl ester (sc-29333) versus aspirin-shock gastric ulcerogenesis in the dog. 679 83

Rats were subjected to severe incomplete cerebral ischemia followed by recirculation. The levels of several of the cyclooxygenase products of arachidonic acid were measured at 5 and 15 minutes of ischemia and at 30 minutes of recirculation following 15 minutes of ischemia, PGE2 accumulated during the first 5 min. of ischemia and its level declined at 15 min. and returned to control level at 30 min. of recirculation. TXB2, on the other hand, increased during the whole time course of the experiment and at the end of the post ischemic period its level was 5 times higher than control. Treatment of the animals with indomethacin (4 mg/Kg, i.v.) prior to ischemia reduced the levels of these products without altering the pattern of their changes. During the ischemic period the EEG was isoelectric and the mean recovery time of electrical cortical activity after 15 min. of ischemia was 10.4 +/- 3.5 min. in the control rats. The rats which received indomethacin recovered faster (43. +/- 0.9 min) and were more resistant to the induction of ischemia. We suggest that the reversibility of cortical activity may be correlated to the accumulation of TXB2 during ischemia and recirculation, and inhibition of its synthesis might improve the post-ischemic reflow.
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PMID:The effect of incomplete cerebral ischemia on prostaglandin levels in rat brain. 689 89

Novel compounds that induce or inhibit platelet aggregation and constrict or dilate blood vessels were recently discovered. These compounds are all derivatives of arachidonic acid and include prostaglandin endoperoxides, thromboxane A2, prostaglandin E2, prostaglandin D2 and prostacyclin. Thromboxane A2 (TxA2) could be one of the precipitating factors in coronary or cerebrovascular ischemia because it is a potent vasoconstrictor that is produced by platelets during their aggregation. On the other hand, prostacyclin (PGI2) is a potent vasodilator and inhibitor of platelet aggregation produced by vessel walls whose enhanced production should be beneficial. Aspirin inhibits prostaglandin endoperoxide synthetase and therefore prevents the subsequent production of TxA2, PGI2 and other prostaglandins. It has been suggested but not yet established that low doses of aspirin preferentially inhibit TxA2 biosynthesis. The roles of classic prostaglandins PGD2, PGE2 and PGF2 alpha in ischemia have not been determined.
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PMID:Thromboxane A2, prostacyclin and aspirin: effects on vascular tone and platelet aggregation. 700 50

Prostaglandins may induce or inhibit platelet aggregation and constrict ro dilate blood vessels. Recent interest has focused on prostaglandins which are derivatives of arachidonic acid including prostaglandin, endoperoxides, thromboxane A2, prostaglandin E2, prostaglandin D2 and prostacyclin. Prostacyclin (PGI2) is a potent vasodilator and inhibitor of platelet aggregation whose enhanced production by vessel walls should be beneficial. It now appears that the circulating levels of PGI2 in man are extremely low and little is known about the manner in which to increase them. Furthermore, aspirin, in doses of as little as 4 mg/kg inhibits prostacyclin as well as thromboxane formation. Thromboxane A2 may be involved in coronary ischemia because it is a potent vasoconstrictor that is biosynthesized during platelet aggregation. Although thromboxane A2 is very unstable indirect evidence obtained by using thromboxane A generating systems or a stable analogue called carbocyclic thromboxane A2 (CTA2) suggests that it exacerbates ischaemic damage because of a selective increase in vascular resistance due to coronary vasospasm and platelet aggregation which acts to decrease myocardial blood flow. The stable prostaglandins PGD2 and PGE2 are also of interest as both are formed during platelet aggregation. Like PGI2, PGD2 inhibits platelet aggregation.
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PMID:Prostaglandins and platelet aggregation. 703 81

In 38 conscious rats divided into seven groups, acute unilateral ischemic renal failure was induced by 1 hour of complete occlusion of the left renal artery while the contralateral kidney remained intact. Renal excretory function of the left kidney was monitored up to 144 hours after ischemia and revealed a typical course of oliguric renal failure with oligoanuria persisting for more than 48 hours. Urinary osmolality and sodium concentration became plasma isotonic after release of renal artery occlusion and approximated control values on day 6 after ischemia. In nine rats, the i.v. infusion of furosemide before (6 microgram/min/100 g body wt) and after (12 microgram/min/100 g body wt) renal artery occlusion protected the ischemic kidney from oligoanuria with endogenous creatinine clearance of 0.42 +/- 0.11 ml/min/g kidney wt 5 hours after ischemia. Tubular absorption of sodium and water was at least partially preserved 36 hours after ischemia when infusion of furosemide was stopped. The loop diuretic significantly (P less than 0.01) increased total urinary prostaglandin (PG) E2 excretion before and after renal artery occlusion; and 5 hours after ischemia, PGE2 excretion from the ischemic kidney significantly exceeded that from the intact kidney (P less than 0.05). Indomethacin (1 mg/100 g body wt) administered in six animals markedly suppressed control PGE2 excretion (P less than 0.05) as well as the furosemide-induced rise in urinary PG excretion before and after ischemia but did not modify the protective effect of the diuretic in this experimental model. Inhibition of PG synthesis, however, reduced urinary flow rate and sodium and potassium excretion of the contralateral intact kidney and almost completely prevented its compensatory rise in creatinine clearance. The results indicate that mechanisms other than the intrarenal prostaglandin system must be considered to mediate the protective effects of furosemide in acute ischemic renal failure.
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PMID:Prostaglandin-independent protection by furosemide from oliguric ischemic renal failure in conscious rats. 739 20

This study examines the hypothesis that acute thermal injury decreases renal and splanchnic vasodilator eicosanoids. Anesthetized rabbits were subjected to sham or a 25% total body surface area burn and fluid resuscitated. At 2, 4, 6, 12, and 24 h postburn the superior mesenteric and renal arteries were cannulated and perfused in vitro with their end organs with Krebs buffer (pH 7.4, 37 degrees C). Renal and splanchnic prostaglandins (PGs) 6-keto-PGF1 alpha (PGI2), and PGE2, and thromboxane B2 (TxB2) release were measured by EIA at 15 min of perfusion. The major eicosanoids released were PGI2 from the splanchnic bed and PGI2 and PGE2 from the kidney. Renal PGE2 and PGI2 and splanchnic PGI2 release were decreased by 50% or more 12 h postburn (p < 0.01) but were restored to sham burn levels 24 h postburn. Loss of these endogenous renal and splanchnic vasodilators 12 h postburn may contribute to ischemia of both vascular beds at this critical time period following acute burn injury.
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PMID:Acute burn down regulates rabbit splanchnic and renal prostanoid release. 748 86

In this experimental study we studied the effect of verapamil and iloprost on endothelin release in ischemia/reperfusion (IR) injury of the rat intestine. Endothelin levels in the portal blood and malondialdehyde (MDA), PGE2, and LTC4 levels in the intestinal tissue were determined. The MDA levels increased in the control group and this increase was reversed with iloprost, verapamil and both. The change in the LTC4 levels was insignificant between the groups. Iloprost reduced PGE2 and endothelin release, but verapamil was not as effective and no synergistic effect was encountered. The increased PGE2/LTC4 ratio was also reversed in the experimental groups, verapamil being less effective. Endothelin release seems to be related to both PGE2 levels and the PGE2/LTC4 ratio after mesenteric IR injury.
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PMID:Effect of verapamil and iloprost (ZK 36374) on endothelin release after mesenteric ischemia-reperfusion injury. 751 92

The implication of different eicosanoids and oxygen free radicals in the development of pancreatic injury after an ischemia-reperfusion process has been evaluated. For this purpose we have compared the effect of allopurinol and indomethacin administration on the pancreatic levels of eicosanoids in a rat model of pancreatic ischemia-reperfusion. After 60 min of pancreatic ischemia and 2 h of reperfusion, significant increases in 6-keto-PGF1 alpha, PGE2, and LTB4 in pancreas tissue were detected. Allopurinol before the ischemic period reduced 6-keto-PGF1 alpha, PGE2, and LTB4 levels to the range of basal values, while prior indomethacin treatment significantly reduced 6-keto-PGF1 alpha and PGE2 levels, with LTB4 remaining unmodified. Increased postischemic plasma lipases were also significantly reduced by allopurinol to the range of sham-operated animals whereas indomethacin did not modify these levels. The data suggest a role for lipoxygenase metabolites in the development of pancreatic injury and the importance of the enzyme xanthine oxidase as an inductor of eicosanoid biosynthesis.
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PMID:Role of xanthine oxidase and eicosanoids in development of pancreatic ischemia-reperfusion injury. 755 51

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

Ergot alkaloids possess some properties potentially beneficial in ischemia of organs. Therefore the effect of pretreatment by nicergoline and bromocriptine was established in ischemia-reperfusion injury of rat liver. PGE2 and verapamil were used as comparative agents. Hepatic ischemia (60 min) of anesthetized rats was induced by clamping of vessels supplying the median and left lateral lobe. Tested drugs were given i.v. 2 or 5 min prior to inducing ischemia. ALT and AST activities in serum two hours after the end of ischemia were used as markers of hepatocellular injury. Only PGE2 (0.1 mg.kg-1) pretreatment minimized the postischemic rise of both ALT and AST activities. Pretreatment with various doses of nicergoline (1 or 4 mg.kg-1), bromocriptine (1 or 4 mg.kg-1) and verapamil (0.9 or 4.5 mg.kg-1) did not influence significantly serum transaminases activities after ischemia. Bromocriptine (4 mg.kg-1) given together with PGE2 did not improve a protective effect against ischemia achieved by the administration of PGE2 (0.1 microgram.kg-1).
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PMID:The effect of pretreatment with prostaglandin E2 (PGE2), verapamil, nicergoline and bromocriptine on ischemia-reperfusion injury of rat liver in vivo. 776 87


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