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

Prostaglandin E1/I2 and insulin receptors of human erythrocyte and platelet are capable of modulating each other's activity. This modulation of the receptor activity and number in one system by a second receptor system in human platelet and erythrocyte seems to be beneficial. Insulin increases the PGE1 binding to platelets and thereby enhances the platelet antiaggregatory action of prostaglandin by increasing cyclic AMP levels. Similarly, PGE1 increases insulin binding to human erythrocyte, and thereby reduces the optimum concentration of insulin for a maximal reduction in membrane microviscosity. During ischemia the reduced response of platelets to the inhibitory effect of PGE1 or PGI2 relates to the impaired PGE1/I2 receptor activity. Treatment of these platelets with insulin at physiological concentrations can normalise the PGE1/I2 receptor activity. This review focuses on the relationship between the two receptor systems in human blood cells.
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PMID:Interaction of receptors for prostaglandin E1/prostacyclin and insulin in human erythrocytes and platelets. 165 91

The responses of 3 patients with systemic lupus erythematosus (SLE) and progressive digital ischemia to intravenous prostaglandin E1 (PGE1) were studied prospectively in an open 3-day trial. All patients were unresponsive to corticosteroids, one had vasculitis proven by biopsy. Digital ischemia diminished in all 3 patients. In one patient, angiograms documented reappearance of a previously obstructed deep palmar arch. Vasospasm plays a role in the outcome of SLE vasculitis even in the absence of Raynaud's phenomenon. As suggested by animal models of necrotizing and leukocytoclastic vasculitis, and by case reports, intravenous PGE1 may be a relatively nontoxic, adjunctive treatment for vasculitis.
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PMID:Reversal of the vasospastic component of lupus vasculopathy by infusion of prostaglandin E1. 178 1

Therapy of chronical arterial occlusive disease primarily includes evaluation and treatment of risk factors as prophylaxis for preventing progression of arteriosclerosis. When patients suffer from claudication walking exercise is the therapy of choice. Only in cases with severe claudication (walking distance under 100 m) and rest pain or ischemic ulcers reopening procedures are necessary. Bypass surgery is supported by the different transluminal angioplasty techniques, which are suited even for the older and multimorbide patients. A pharmacological treatment of peripheral arterial occlusive disease should be introduced only for preventing progression of the disease or reocclusions following surgery or angioplasty or in those cases in whom reopening techniques are not possible or not successful. Here prostaglandin E1 has been proven to be effective in many clinical trials. The combination of surgery, angioplasty and pharmacological treatment allows to avoid major amputations in most patients with critical limb ischemia.
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PMID:Prostanoids in therapy of peripheral arterial occlusive disease. 179 58

The blood levels of 6-keto-PGE1 alpha and thromboxane B2 were measured in the coronary sinus of 15 males during and just after a spontaneous myocardial ischemic episode. The comparison was made in 30 males with coronary heart disease in the presence of exercise-induced angina in whom coronary sinus blood samples were taken during myocardial ischemia provoked by pacing and 6 males suffering from cardialgias without signs of coronary atherosclerosis. The patients with spontaneous anginal attacks had lower baseline 6-keto-PGE1 alpha (179.0 +/- 47.8 pkg/ml) than those with exercise-induced angina (336.0 +/- 65.7 pkg/ml; p less than 0.1). This difference became greater during ischemia (165.0 +/- 49.0 and 350.0 +/- 69.5 pkg/ml, respectively, p less than 0.05) and just after its elimination (166.0 +/- 48.7 and 413.0 +/- 76.0 pkg/ml, respectively, p less than 0.05). Coronary sinus blood thromboxane B2 levels were not substantially different in the presence or absence of myocardial ischemia. Thus, a decrease in the prostacyclin-forming function of the coronary endothelium plays a definite role in the genesis of spontaneous myocardial ischemic episodes.
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PMID:[Coronary sinus blood thromboxane and prostacyclin in spontaneous myocardial ischemia]. 179 81

Effects of treatment with prostaglandin E1 (PgE1) on normothermic liver ischemia were studied in male Lewis rats. Animals were subjected to 90 min of warm liver ischemia. Two groups of rats were constituted: group A (no treatment) and group B (PgE1 treatment). PgE1 (100 micrograms/kg) was given as a bolus 2 min before induction of ischemia and 2 min before the end of ischemia. Survival rates were assessed and, 6 h after the end of ischemia, serum transaminases, histology of the liver, Kupffer cell activity were evaluated. PgE1 treatment significantly improved survival rate (80%) in comparison with the nontreated group (40%). A significant reduction in transaminase levels was observed after PgE1 The extent of necrosis and congestion was improved by PgE1 treatment. Sheep red blood cell 51Cr liver uptake was deeply depressed 6 h after the end of ischemia in group A (6 +/- 2.3%/g tissue), and was significantly higher (p less than 0.001) after PgE1 administration in group B (32.98 +/- 11.7%/g tissue). Our results demonstrate that PgE1 is able to protect the liver from ischemic insult. The mechanism by which prostaglandins exert this beneficial effect on normothermic liver ischemia may be related to their action on hepatic macrophages.
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PMID:Protective effects of prostaglandin E1 on normothermic liver ischemia. 180 30

The importance of right ventricular (RV) function in maintaining global cardiac performance is the focus of this discussion. The physiological determinants of normal right ventricular function will be discussed, with particular emphasis on the afterload and contractility characteristics of the right ventricle. Numerous clinical conditions have been shown to affect RV performance. These conditions include positive-pressure ventilation, ischemia, pulmonary hypertension, and cardiac surgery. Present methods for the perioperative evaluation of RV function include angiography, radionuclide techniques, thermodilution techniques, echocardiography, and magnetic resonance imaging. Traditional modalities for the treatment of RV dysfunction consist of pharmacological interventions (i.e., vasodilators and inotropes) and/or mechanical assist devices. Newer pharmacological strategies for the treatment of RV failure and associated pulmonary hypertension include the phosphodiesterase fraction III inhibitors and the prostaglandins, specifically PGE1. In summary, the accurate evaluation of perioperative RV performance combined with new treatment options will ensure maximal preservation of RV performance.
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PMID:Right ventricular function and failure: a review. 181 51

Therapy of chronic arterial occlusive disease primarily includes evaluation and treatment of risk factors as prophylaxis for preventing progression of arteriosclerosis. When patients suffer from claudication walking exercise is the therapy of choice. Only in cases with severe claudication (walking distance under 100 m) and rest pain or ischemic ulcers reopening procedures are necessary. Bypass surgery is supported by the different transluminal angioplasty techniques, which are suited even for older and multimorbid patients. A pharmacological treatment of peripheral arterial occlusive disease should be introduced only for preventing progression of the disease or re-occlusions following surgery or angioplasty or in those cases in whom reopening techniques are not possible or not successful. Here prostaglandin E1 has been proven to be effective in many clinical trials. The combination of surgery, angioplasty and pharmacological treatment allows to avoid major amputations in most patients with critical limb ischemia.
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PMID:[Therapy of peripheral arterial occlusive disease with special reference to prostaglandins]. 182 25

Interruption of hepatic blood supply for 60 min deteriorated liver mitochondrial respiratory functional indices--that is, respiratory control index (RCI) and the rate of oxygen consumption in state-III respiration (ST III O2). Recovery of ischemia-induced decreases in these functional indices in a saline-administered cirrhotic liver group was retarded compared with that in a normal liver group, and significantly low RCI and ST III O2 persisted 15 min after reperfusion. Prostaglandin E1 (PGE1) did not improve ischemia-induced decreases in RCI and ST III O2 but accelerated the recovery of mitochondrial respiratory function after reperfusion. Adenosine triphosphate (ATP) levels were markedly decreased during ischemia, and retardation of ATP recovery was also observed in rats with cirrhosis. PGE1 improved the recovery of ATP level in rats with cirrhosis. Liver blood flow in the cirrhotic liver was significantly lower than that of the normal liver. PGE1 enhanced liver blood flow. These results indicate that retardation of the recovery of RCI and ST III O2 in the cirrhotic liver might be based on the decrease in tissue blood flow and that agents increasing tissue blood flow might contribute to the acceleration of the recovery of mitochondrial respiratory function.
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PMID:Effects of prostaglandin E1 on the recovery of ischemia-induced liver mitochondrial dysfunction in rats with cirrhosis. 185 49

Two ester-type prostaglandin oligomeric compounds were synthesized, one from prostaglandin E1 (termed MR-356) and the other from prostaglandin B2 (termed OC-5186). Using in vivo [31P]MRS, the protective effects of these oligomers on forebrain ischemia (15 min) were evaluated in a rat model. Forebrain ischemia caused a decrease in intracellular high energy phosphates and intracellular pH (pHi) in the control and compounds-treated groups, but changes of these values in the OC-5186-treated group were significantly smaller than those in the control group. Moreover, the cerebral energy metabolism of the OC-5186-treated group returned to the preischemia level more rapidly than in the control group after forebrain ischemia. MR-356 had some effects, but the differences were not significant.
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PMID:[31P]MRS study of the protective effects of prostaglandin oligomers on forebrain ischemia in rats. 186 52

The effects of hydralazine and prostaglandin E1 on regional myocardial function were studied in dogs. Sixteen dogs were randomly assigned to one of two drug treatment groups of eight dogs each. The first group (G1) was treated with 0.4 mg/kg hydralazine administered as a bolus. The second group (G2) received prostaglandin E1 given as an infusion for a total dose of 0.8 micrograms/kg. Regional myocardial function was assessed through the measurement of myocardial segment shortening during systole. We call this index percent systolic shortening (%SS). An ischemic heart preparation was created by partial occlusion of coronary blood flow. The degree of induced ischemia was determined by following the reduction in %SS. Hydralazine reduced %SS of the ischemic myocardium while increasing the cardiac index, stroke volume index, and coronary blood flow. Prostaglandin E1 increased %SS, cardiac index, and stroke volume index in the ischemic heart preparation. Hydralazine, therefore, induced dissociation between global ventricular function and regional myocardial function whereas prostaglandin E1 did not. The present findings emphasize that evaluation of vasoactive drugs should consider their effects on regional myocardial function as well as on global hemodynamics.
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PMID:Effects of hydralazine and prostaglandin E1 on regional myocardial function in the ischemic canine heart. 198 67


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