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 objective of this study was to determine whether or not a relationship exists between free fatty acid (FFA) extraction by skeletal muscle and onset of irreversible shock. Hind limb skeletal muscle vasculature of anesthetized dogs was surgically isolated from cutaneous tissue and subjected to a modified Wigger's hemorrhage shock protocol which was divided into five stages (I-V). Since the first signs of irreversibility began in stage II, this stage of hypovolemic hypotension was subdivided into IIa, IIb and IIc. Arterial and venous blood samples were taken during each stage for subsequent blood gas and FFA analysis. The data indicated that the onset of severe tissue ischemia and metabolic acidosis occurs concurrently with increased uptake of FFA and skeletal muscle vasodilation (decompensation). A possible physiological explanation for these observations could be related to an increased synthesis and release of PGE1. This agent has been shown by others to inhibit adrenergic neurotransmitter release causing loss of vascular tone.
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PMID:Correlation between skeletal muscle free fatty acid extraction and vascular decompensation during hemorrhagic hypotension. 50 62

A comparison study of several vasoconstrictor and vasodilator agents was conducted measuring changes in intestinal blood flow and oxygen consumption during 10-min periods of intra-arterial infusion. Blood flow was measured in a branch of the superior mesenteric artery of anesthetized dogs with an electromagnetic blood flow meter, and the arteriovenous oxygen content difference across the gut segment was determined photometrically. Vasopressin (4 x 10(-3) and 7x 10(-4) U/kg-min) diminished blood flow 60 and 28% and reduced oxygen consumption 54 and 22%, respectively (all P less than 0.001). In a dose which did not lower blood flow, vasopressin still caused a decline in oxygen consumption (P less than 0.01). Epinephrine (5 x 10(-2) mug/kg-min) decreased blood flow 19% (P less than 0.001) but did not reduce oxygen consumption. After beta-adrenergic blockade, however, the same dose of epinephrine decreased blood flow 41% and oxygen consumption 33% (both P less than 0.001). Responses to angiotension II, calcium chloride, and prostaglandin F2alpha resembled effects of vasopressin rather than those of epinephrine, namely decreased blood flow and decreased oxygen consumption. The vasodilator agents, prostaglandin E1, is isoproterenol, and histamine, increased (P less than 0.001) both blood flow (130, 80, and 98%, respectively) and oxygen consumption (98, 64, and 70%, respectively). Vasopressin, angiotensin II, calcium chloride, and prostaglandin F2alpha appear to contract arteriolar and precapillary sphincteric smooth muscle indiscriminately to evoke both intestinal ischemia and hypoxia. Epinephrine is the exceptional constrictor in this case, producing diminished blood flow without a reduction in oxygen uptake.
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PMID:Effect of vasoactive agents on intestinal oxygen consumption and blood flow in dogs. 115 Aug 81

Nonocclusive mesenteric ischemia was produced in dogs by intraarterial infusion of digoxin and by hemorrhage of 1/3 of total blood volume. Both methods produced a substantial drop in the superior mesenteric arterial blood flow rate. In each case, a superior mesenteric arterial infusion of 0.1 mug./kg. per minute of prostaglandin E1 allowed the blood flow rate to increase to above the control level without significantly altering heart rate or systemic arterial pressure. The improved arterial blood flow rates were accompanied by a reversal of the diffuse mesenteric vasoconstriction that was seen in the ischemic state. These findings were demonstrated by superior mesenteric arteriography performed prior to and following the production of mesenteric ischemia and again following the infusion of prostaglandin E1.
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PMID:Experimental use of prostaglandin E1 in nonocclusive mesenteric ischemia. 120 Feb 25

The inhibition of lipid peroxidation by oligomeric derivatives synthesized from prostaglandin E1 (PGE1) and PGB2 was studied using two rat models. In an in vitro model, the brain was exposed to decapitation-ischemia, the cortex was removed and homogenized, and the formation of thiobarbituric acid reactive substances (TBAR) was measured after exposing the homogenate to in vitro reoxygenation either in the presence or absence of oligomers. It was found that these oligomers could inhibit lipid peroxidation, and that their activities were higher than that of superoxide dismutase (SOD). In an in vivo administration model, either the oligomer or the vehicle was injected i.p. 30 min before decapitation. The brain was exposed to decapitation-ischemia, the cortex was homogenized and exposed to 'in vitro' reoxygenation, after which TBAR value was determined. Ester-type compounds had a greater activity than free-acid type compounds in inhibiting lipid peroxidation. A possible mechanism of the protective effect of these oligomers in ischemia/reperfusion injury may be to scavenge oxygen free radicals.
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PMID:Inhibition of lipid peroxidation by prostaglandin oligomeric derivatives. 131 35

Metabolic disturbances in the canine liver during warm ischemia by Pringle's method for 60 minutes and the role of Coenzyme Q10 (CoQ10), Prostaglandin E1 (PGE1) and ONO-3708, TXA2 receptor antagonist, were studied. Mongrel dogs were divided into five groups; control group, group of liver ischemia without drugs, groups of liver ischemia with CoQ10, PGE1 and ONO-3708 pretreatment. Metabolic rates of PGI2, TXA2, insulin, glucagon and glucose and production of lipid peroxides in the five groups were measured at the points before Pringle's procedure, 5 minutes, 60 minutes and 120 minutes after declamping. In the group of ischemia without drug administration, the hepatic metabolism of PGI2, TXA2, insulin and glucose were decreased after declamping. The metabolism of glucagon, however, was not disturbed by warm ischemia. The production of lipid peroxides increased at 5 minutes after declamping. In the groups of CoQ10, PGE1 and ONO-3708 pretreatment, changes of PGI2, TXA2 and insulin metabolism in the liver were improved, and an increased production of lipid peroxides by warm ischemia was normalized. This study suggests that CoQ10, PGE1 and ONO-3708 protect liver damage by warm ischemia as results of improvement of metabolic disturbances of PGI2, TXA2, insulin and suppression of lipid peroxides production.
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PMID:[Assessment for protective effects of CoQ10, PGE1 and TXA2 receptor antagonist (ONO-3708) on warm ischemic liver]. 138 60

The ability of prostaglandins to protect the kidney against ischemic and toxic renal injury was evaluated by in vivo and in vitro models of renal ischemia. The prostaglandin E1 analogue, misoprostol, was found to provide significant protection against ischemia-induced renal dysfunction in rats subjected to 40 minutes of renal artery occlusion. Misoprostol-treated rats had glomerular filtration rates almost threefold greater than control animals, although renal blood flow and renal vascular resistance were not significantly different. Improved tubular function was reflected in a lower fractional excretion of sodium and a higher urine-to-plasma creatinine ratio. Misoprostol also provided similar protection in a model of toxic renal injury produced by mercuric chloride. In an in vitro model employing primary cultures of proximal tubule epithelial cells subjected to hypoxia and reoxygenation, misoprostol limited cell death. Posthypoxic cells had apical membrane disruption and loss of microvilli when examined by transmission electron microscopy. These changes were not seen in misoprostol-treated cells. The "cytoprotective" effect was also produced by prostaglandin E2 and prostacyclin. The ability of prostaglandin E to protect against toxic and ischemic renal injury did not appear to be due to an antioxidant effect because misoprostol did not limit lipid peroxidation in vivo and did not protect against oxidant injury by tert-butyl hydroperoxide in vitro. Although the exact mechanism of prostaglandin protection was not revealed, these studies demonstrate that prostaglandins protect renal tubule epithelial cells from hypoxic injury at the cellular level independent of hemodynamic factors or inflammatory responses. Such a "cytoprotective" effect of prostaglandins may be a generalized phenomenon since it has also been demonstrated in gastrointestinal epithelium.
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PMID:Prostaglandins protect kidneys against ischemic and toxic injury by a cellular effect. 147 66

The hepatoprotective effects of misoprostol, a PGE1 analog, against ischemia-reperfusion liver injury were studied using a rat partial liver ischemia model. Serum ornithine carbamoyltransferase (OCT) and alanine aminotransferase (ALT) levels were determined as biochemical indices of injury. Hepatic cell necrosis was assessed histologically using tetranitroblue tetrazolium (TNBT) and hematoxylin and eosin (H&E) staining. With placebo treatment, 90 min of partial hepatic ischemia followed by 24 hr of reperfusion resulted in increased levels of serum OCT (760 +/- 521 IU/liter) and ALT (4327 +/- 1982 IU/liter), while extensive hepatic necrosis was evident by TNBT and H&E staining. Treatment with two doses of 25 micrograms misoprostol/kg body weight at 1 min before ischemia and 1 min before reperfusion significantly reduced the serum levels of OCT and ALT (207 +/- 189 IU/liter, P less than 0.01 and 2075 +/- 1217 IU/liter, P less than 0.01, respectively) and hepatic necrosis. When a single dose of misoprostol was administered 1 min before reperfusion, similar protective effects were observed. However, when the treatment of misoprostol was delayed to 1 min after reperfusion, significantly less hepatoprotection was seen. Misoprostol exerted no hepatoprotection at all when it was administered at 5 min or later after reperfusion. These results demonstrate that misoprostol partially protects the liver against ischemia-reperfusion injury in the rat. The observation that the protective effect of misoprostol occurs only within the first minute of reperfusion suggests that its mechanism of action involves an early event in reperfusion injury, such as modifying the effects of reactive oxygen metabolites.
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PMID:Misoprostol hepatoprotection against ischemia-reperfusion-induced liver injury in the rat. 149 53

The change of liver lysosomal enzymes in tissue and serum during a reperfusion period was studied in partial liver ischemic model in rats and effect of Prostaglandin E1 (PGE1) derivative on partial liver ischemia was investigated. Partial liver ischemia was induced by clamping the branches of the vessels to the right and caudate lobes of rat liver. The clamp was released after 30 minutes of ischemia. Ischemic and nonischemic lobes of the liver were separately removed and the serum was also collected immediately and two hours after the release of the clamp. Lysosomal enzyme activities from free and bound lysosomal fraction were measured separately and the fragility index (F.I.) was calculated. PGE1 derivative was administered intraperitoneally 24, 6, 0.5 hours prior to the induction of ischemia at each dose of 0.05 microgram/kg. Pretreatment with PGE1 derivative prevented lysosomal labilization in ischemic lobe, since there was a significant decrease in F.I. of cathepsin D in the PGE1-pretreated group (preischemia; 28.3 +/- 2.4%, immediately after reperfusion; 30.3 +/- 2.5%, two hours after reperfusion; 30.3 +/- 2.5%) compared to the placebo group (immediately after reperfusion; 40.9 +/- 3.4%, two hours after reperfusion; 41.7 +/- 3.4%, p less than 0.05, p less than 0.05, p less than 0.01, respectively). Pretreatment with PGE1 derivative also significantly suppressed the increase of serum lysosomal enzyme activity. These results showed that PGE1 derivative improved liver lysosomal labilization in partial liver ischemia.
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PMID:[Effect of prostaglandin E1 derivative on labilization of liver lysosomal membrane in partial liver ischemia]. 151 9

In recent years, the number of elderly patients who require operation has been increasing. We experienced three patients with perioperative brain infarction, occurring respectively, during the preoperative period, just after operation, and three days after operation. All three patients had more than one of the common risk factors for cerebrovascular accidents, including hypertension, advanced age, hyperfibrinogenemia, diabetes mellitus, and past history of cerebrovascular accident. On the basis of our experience with these three patients, we suggest the following: (1) Waiting period of elective surgery should be reconsidered in some cases with a past history of stroke. (2) Some high-risk patients may benefit from anticoagulative or antiaggregative drugs (e.g. low-molecular dextran or prostaglandin E1) to prevent brain ischemia. (3) Abrupt control of hypertension or diabetes mellitus status undoubtedly adversely affects the patient's general condition; and (4) A practical monitoring system to detect regional brain ischemia during operation under general anesthesia should be developed.
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PMID:[Three cases of perioperative brain infarction]. 156 May 89

Pulmonary vasodilator therapy during increased right ventricular (RV) afterload and insufficient RV myocardial perfusion might further impair RV performance by lowering systemic and, thus, coronary perfusion pressure. This hypothesis was tested by initially inducing pulmonary hypertension (80% increase in resting pulmonary artery pressure by injection of autologous muscle) and subsequent right coronary artery stenosis (40% decrease in flow by external cuff occlusion) in eight open-chest dogs. Then the effects of nitroglycerin (5 micrograms.kg-1.min-1), prostaglandin E1 (0.2 microgram.kg-1.min-1), and hydralazine (mean 0.14 mg/kg) on global and regional (ultrasonic dimension technique) RV performance and coronary hemodynamics (electromagnetic flow probes) were determined. Following all three drugs, right coronary artery flow decreased by 40-65% (mean values) accompanied by severe regional myocardial dysfunction suggestive of ischemia (akinesis, systolic lengthening, and postsystolic shortening). Heart rates increased by 20-40%; aortic pressure decreased by 15-25%; and RV end-diastolic pressure remained unchanged. Despite similarly adverse effects on regional RV performance and comparable effects on heart rate, perfusion and filling pressures with all three drugs, RV systolic pressure, RV dP/dt, and pulmonary artery pressure during nitroglycerin and prostaglandin E1 remained unchanged, and stroke volume and pulmonary artery flow decreased, but they all increased or were maintained (stroke volume) during hydralazine. Gas exchange was not affected by any of the vasodilators. Thus, in this model of combined acute pulmonary hypertension and right coronary artery insufficiency, nitroglycerin, prostaglandin E1, and hydralazine elicited severe regional dysfunction suggestive of ischemia, probably related to concomitant increases in heart rate and decreases in coronary perfusion pressure. Despite such evidence of severe regional RV ischemia, hydralazine maintained global RV pump function. These results indicate 1) that in the presence of increased RV afterload and coronary insufficiency, reduction in coronary perfusion pressure during pulmonary vasodilator therapy may be deleterious, and 2) that even severe regional myocardial ischemia may not necessarily be accompanied by respective changes in global hemodynamics and thus may go undetected.
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PMID:Myocardial ischemia during vasodilator therapy in a canine model of pulmonary hypertension and coronary insufficiency. 157 47


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