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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We found recently that exogenously administered PGD2, PGE1 and PGI2 showed a protective effect against cerebral hypoxia/ischemia in mice. In the present study, to find out whether these PGs play a pathophysiological role in cerebral hypoxia/ischemia, we examined a possible role of PGs in the development of adaptive protection against cerebral hypoxia/ischemia. Mice were pretreated with a sublethal dose of KCN, hypoxic gas mixture and electroshock 10-120 min before tests. Ten to thirty min after pretreatment with a sublethal dose of KCN, mice proved to be significantly protected against cerebral hypoxia/anoxia in all models studied: KCN-induced anoxia, normobaric hypoxia and decapitation-induced gasping. Similar results were observed when hypoxic gas and electroshock were used as pretreatments. These facts indicate that the protective effect does not depend on how cerebral hypoxia/anoxia is induced but on the substances formed in the brain after hypoxia/anoxia as well as electroshock. Brain concentrations of cyclooxygenase products markedly increased subsequent to hypoxia/anoxia as well as electroshock. The increase in PGs formation as well as resistance to hypoxia was prevented by pretreatment with indomethacin. These findings suggest that endogenously formed PGs at least including the three PGs, PGD2, PGE1 and prostacyclin in mouse brain during or after hypoxia/ischemia are responsible for the increase of resistance to hypoxia/ischemia.
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PMID:A possible role of endogenously formed cerebral prostaglandins in the development of adaptive protection against cerebral hypoxia/ischemia in mice. 344 51

Pretreatment with the thromboxane synthase inhibitor OKY-046 but not the cyclo-oxygenase inhibitor ibuprofen protects against ischemia-induced acute tubular necrosis. However, ibuprofen together with the vasodilating agent prostaglandin E1 is protective. This suggests that a high prostaglandin to thromboxane ratio is the major factor operative in preventing tubular necrosis, the subject of this study. Rats that had unilateral nephrectomy (n = 60) with the exception of rats that had sham operations (n = 8) underwent 45 minutes of left renal pedicle clamping. Thirty minutes before the operation, the rats received either a saline solution or a thromboxane synthase inhibitor that was given intravenously. The inhibitors OKY-046 (2 milligrams per kilogram, n = 10), UK38485 (1 milligram per kilogram, n = 9) and U63357A (10 milligrams per kilogram, n = 10) were given as a single bolus while the inhibitor CGS13080 (0.1 milligram per kilogram, n = 9, and 1.0 milligram per kilogram, n = 7) was given by constant infusion and continued for 60 minutes after reperfusion. With saline solution therapy, five minutes after reperfusion, thromboxane B2 increased from 154 to 2,537 picograms per milliliter (p less than 0.00001) and 6-keto-prostaglandin F1 alpha increased from 51 to 266 picograms per milliliter (p less than 0.004). At 24 hours, the creatinine level increased from 0.5 to 2.8 milligrams per deciliter (p less than 0.00001). Only OKY-046 yielded a creatinine level at 24 hours of 1.2 milligrams per deciliter, a value lower than that for those in the saline solution control group (p less than 0.002). Furthermore, OKY-046 led to the highest prostaglandin to thromboxane ratio (p less than 0.035). The five other ratios which occurred after drug therapy were inversely related to the decrease in the creatinine value (r = -0.93, p less than 0.02). Histologically, OKY-046 was the only thromboxane synthase inhibitor to prevent acute tubular necrosis (p less than 0.05). Results show that a high prostaglandin to thromboxane ratio protects against acute tubular necrosis.
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PMID:A high plasma prostaglandin to thromboxane ratio protects against renal ischemia. 367 99

Thromboxane (Tx) synthase but not cyclo-oxygenase inhibitors prevent acute tubular necrosis (ATN) after renal ischemia, a phenomenon believed to be due to stimulation of the endogenous production of vasodilating prostaglandins (PG). This study directly tests that vasodilating PG protect against the consequences of renal ischemia. Anesthetized, 500-g rats had right nephrectomy and 45 minutes of left renal pedicle clamping or sham clamping. The rats were treated with intravenous (I.V.) saline 1.9 mL/h starting 40 minutes after clamping or sham clamping. All rats except the sham group (N = 8) were pretreated 1 hour before ischemia with ibuprofen (12 mg/kg) to prevent prostanoid synthesis. Beginning 5 minutes before clamp release, the rats were treated intravenously for 2 hours with: saline vehicle (N = 9), PGE1 400 ng/kg/min (N = 6), nitroprusside 4 micrograms/kg/min (N = 8), or dopamine 3 micrograms/kg/min (N = 11). After 24 hours, sham rat creatinine level was 0.5 mg/dL and weight of the left kidney was 86.5% of the previously removed right kidney. Compared with sham rats, ischemia and saline treatment resulted in a rise in creatinine level to 2.7 mg/dL (p less than 0.05) and a rise in kidney weight to 101.9% (p less than 0.05); PGE1 led to a creatinine level of 1.1 mg/dL, a value lower than that of the rats treated with saline (p less than 0.05), and a kidney weight of 92.0%, a value similar to that of sham rats; nitroprusside and dopamine led to a rise in creatinine levels to 3.2 mg/dL (p less than 0.05) and 2.3 mg/dL (p less than 0.05), respectively, as well as a rise in kidney weight to 108.0% (p less than 0.05) and 105.4% (p less than 0.05), respectively. Histologic examination showed ATN in rats treated with saline, nitroprusside, and dopamine, but not in rats treated with PGE1. These results indicate that PGE1 protects the cyclo-oxygenase-treated kidney against ischemia-induced ATN.
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PMID:Vasodilator prostaglandins (PG) prevent renal damage after ischemia. 381 90

Effect of 48-72 hour infusion of prostaglandin E1 (PGE1) was studied in 17 patients with angina refractory to conventional medical treatment (combination of propranolol, 160 mg/day nifedipin, 30 mg/day and nitrates) by the double blind test. PGE1 was infused to 11, placebo to 6 patients. There was no difference between PGE1 and placebo groups in the number of ischemic episodes and duration of myocardial ischemia as evidenced by Holter ECG monitoring. But in 2 patients with vasospastic angina attacks of ischemia were almost completely abolished by PGE1.
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PMID:[Infusion of prostaglandin E1 in resting angina resistant to conventional therapy]. 390 82

The protective effect of intravenous administration of exogenous prostaglandin E1 on ischemia-induced acute renal failure was investigated in dogs. The parameters studied were renal cortical blood flow, renal function, survival time, and histologic changes. The model was prepared by clamping the renal artery for 1 or 2 hours. Renal cortical blood flow was measured by the hydrogen washout technique. After prostaglandin E1 administration, renal cortical blood flow increased significantly and renal function was maintained at relatively high levels with low serum creatinine and moderate creatinine clearance levels. Mean survival time increased markedly from 4.1 to 35.2 days by administration of prostaglandin E1. Ischemia-induced acute renal failure is usually accompanied by zonal necrosis of renal tubules prominent in the cortex. However, occurrence of these histologic damages could be virtually prevented by prostaglandin E1 administration (i.e., only minimal tubular necrosis was found in a small area of the cortex). We conclude from this study that postischemic administration of exogenous prostaglandin E1 does provide a certain degree of protection for the kidney, which may have a great clinical implication in improving the success rate of kidney transplantation, especially of cadaver donor kidneys.
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PMID:Protective effect of prostaglandin E1 on ischemia-induced acute renal failure in dogs. 404 Feb 71

Prostaglandins in concentrations too low to stimulate afferent nerve endings in the heart may sensitize them to chemical or mechanical stimuli that activate cardiac reflexes during myocardial ischemia. Bradykinin, which is released from the heart during ischemia, elicits sympathetically mediated reflex pressor effects and tachycardia when applied in low doses (0.1 to 1 microgram) to the epicardium of the left ventricle in open-chest, anesthetized dogs. The reflex pressor effects evoked by bradykinin are reduced after inhibition of prostaglandins biosynthesis with indomethacin and potentiated by concomitant topical application of low doses (0.1 to 0.3 microgram/min) of PGE1 or PGE2 and prostacyclin (PGI2). The pressor and tachycardic responses to bradykinin are also enhanced after temporary (10-minute) coronary occlusion; this potentiation is abolished by indomethacin treatment and can be restored by superfusing the ventricle with prostaglandins. Nicotine is known to excite mechanosensitive vagal receptors with afferent C fibers, which supply the left ventricle, and to elicit reflex hypotension and bradycardia. This depressor vagal reflex evoked by epicardial or intracoronary administration of nicotine (10 to 50 micrograms) was not affected by either indomethacin or by topical application of PGE1, PGE2, or PGI2. Also, intracoronary infusion of PGE2 (0.1 to 0.3 microgram/min), which enhanced the pressor reflex effects of bradykinin, was without effect on nicotine-induced depressor reflex. However, intracoronary infusion of PGI2 (0.1 to 0.3 microgram/min) significantly enhanced the hypotensive and bradycardic responses to nicotine and, at the same time, reduced sympathetically mediated reflex effects of bradykinin. The hypotensive effects induced by epicardial or intracoronary administration of nicotine were also significantly enhanced during intravenous infusion of subdepressor doses of PGI2 (5 to 20 ng/kg/min). Treatment with captopril, which enhances the endogenous production of prostaglandins, greatly enhanced the reflex depressor effects of nicotine; this potentiating effect of captopril was completely abolished by indomethacin treatment. An increase in the magnitude of nicotine-induced reflex depressor effects was also observed after intravenous injection (1 microgram/kg) or infusion (25 to 50 ng/kg/min) of prostaglandin D2. A working hypothesis is proposed to account for the role of prostanoids in activation of cardiac reflexes during myocardial ischemia.
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PMID:Prostanoids and cardiac reflexes of sympathetic and vagal origin. 634 52

Out of sixty patients with thromboangitis obliterans from January 1966 to December 1981, 50 cases underwent such surgery as sympathetic ganglionectomy, thromboendarterectomy and arterial bypass. The remaining 10 cases received conservative therapies such as intravenous infusion of Prostaglandin E1 (60 micrograms in 5% glucose 500 ml) and epidural sympathetic ganglion block using 1% xylocaine. Good results were obtained in 29 operative cases and in 5 cases with non-surgical therapies. Among the operative cases, the subjective symptoms after discharge improved in forty-one patients (82%) unchanged in three (6%) and remained poor in six (12%). While, those of non-surgical group improved in eight and unchanged in two. In twelve of twenty-nine operative patients whose subjective symptoms improved immediately after discharge, their subjective distress turned worse again. However, the subjective symptoms of 5 patients in non-surgical group remained well in follow-up studies. Many patients who were diagnosed unchanged during follow-up period, had underwent the lumbar and/or thoracic sympathetic gangloinectomy. It is thus concluded that the effects of the sympathetic ganglionectomy are not permanent. The arterial reconstructive surgery is very effective for relief of peripheral ischemia in the follow-up studies if good function of the grafts was obtained in the early postoperative period.
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PMID:[Evaluation of surgical therapy for thromboangitis obliterans, with special reference to follow-up studies]. 667 98

This study evaluates the effects of Indomethacin (IND), Prostaglandin E1 (PGE1), and Ibuprofen (IBP) in a bowel ischemia model. Laparotomy was performed in 80-gram rats (n = 260). Transient ischemia was induced by a one minute occlusion of the superior mesenteric artery. Animals were placed in five experimental groups: (I) ischemic controls (n = 80), (II) PGE1, 80 micrograms/kg IV (n = 20), (III) IBP, 12.5 mg/kg IV (n = 60), (IV) IND 15 mg/kg IV (n = 80) and (V) PGE1 + IND (n = 20). All medications were given just prior to laparotomy. Animals were evaluated for survival, length of survival and the presence of bowel necrosis and/or perforation at seven days. Survival was 18% in controls and was reduced to 5% by IND (p less than .005). Improved survival was observed with PGE1 (35%), TBP (31%) and PGE1 + IND (35%). IND resulted in early death, while PGE1, IBP, and PGE1 + IND all increased the length of survival (p less than .05). IND-treated rats had a high incidence of bowel perforation (greater than 40%). PGE1 reversed this effect when given concomitantly with IND. IBP had a significantly lower incidence of intestinal necrosis. These data suggest that infants treated with IND who are at risk for NEC should be carefully monitored for evidence of bowel necrosis. PGE1 and IBP may have a cytoprotective role in subjects at risk for bowel ischemia.
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PMID:Comparative effects of indomethacin, prostaglandin E1, and ibuprofen on bowel ischemia. 668 9

PGE1 appears to act as a physiological regulator of uteroplacental blood flow. Its vasodilatory, anti-vasopressor, and platelet stabilizing effects could be expected to counteract the placental ischemia, hypertension and excessive coagulation that are seen in pre-eclampsia. Supplementation with efficient essential fatty acid precursors of PGE1 reduces platelet aggregation, has been used with success in the treatment of hypertension and arterial vasospasm, and might offer a nutritional means of reducing the incidence and severity of pre-eclampsia. Assurance of adequate general nutrition also appears to be of importance in this regard.
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PMID:Nutritional prevention of pre-eclampsia--a special role for 1 series prostaglandin precursors? 689 Jun 22

Prostaglandin E1,PGD2, and 16,16 dimethyl prostaglandin E2 were studied in an isolated perfused cat heart preparation during normal conditions and in myocardial ischemia. Under ischemic perfusion, prostaglandin E1 showed some protective action on the release of creatine kinase into perfusate during ischemia, but none of the prostaglandins studied prevented increases in perfusate creatine kinase after reperfusion. Prostaglandin E1 also showed significant membrane stabilizing activity reducing the rate of lysosomal hydrolase release from cat liver lysosomes. Prostaglandin E1 may be beneficial in myocardial ischemia due to its membrane stabilizing action and perhaps to other effects but it did not exert significant protective effects on reperfusion injury of the ischemic myocardium under conditions of these experiments.
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PMID:Cardiac effects of prostaglandins during global ischemia in isolated perfused cat hearts. 695 73


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