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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In helically cut strips of dog cerebral, coronary, mesenteric and femoral arteries, the contractile response to prostaglandin (PG) F2alpha, and E2, relative to contractions induced by 30 mM K+, did not appreciably differ, whereas relaxations induced by PGE1 relative to those induced by 10(-4) M papaverine were significantly different; the least in cerebral arteries and the greatest in mesenteric arteries. The relaxation of human cerebral arteries in response to PGE1 was similar to that of dog cerebral arteries. Treatment for 60 min with polyphloretin phosphate (3 X 10(-5) and 10(-4) g/ml) suppressed the contractile response to PGF2alpha and E2 but did not alter the response to 25 mM K+. The relaxing effect of PGE1 was not influenced. Aspirin (5 X 10(-5) and 2 X 10(-4) M) significantly potentiated the contractile response to PGF2alpha and E2 but did not alter the relaxation induced by PGE1. In contrast, contractions induced by serotonin were attenuated. It is concluded that dog cerebral, coronary, mesenteric and femoral arteries relaxed differently in response to PGE1. It appears that arterial responses to vasoconstricting PGs, but not to the vasodilating PG, are significantly attenuated by polyphloretin phosphate and potentiated by aspirin.
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PMID:Responses of isolated dog cerebral and peripheral arteries to prostaglandins after application of aspirin and polyphloretin phosphate. 70 32

The effects of prostaglandin E1 on pulmonary circulation and left ventricular performance have been studied in 20 patients with mitral valve disease and pulmonary hypertension. Prostaglandin E1 was administered intravenously over a period of 30 minutes. The dose used was 0.01 microgram/kg per min during the first 15 minutes and 0.02 microgram/kg per min subsequently. The first dose led only to an insignificant fall in left ventricular end-diastolic pressure. Infusion of prostaglandin E1 in a dose of 0.02 microgram/kg per min resulted in a significant fall in the pulmonary arterial pressure (P less than 0.001), total pulmonary resistance (P less than 0.001), left ventricular end-diastolic pressure (P less than 0.001), and aortic pressure (P less than 0.01), and an increase in the pulmonary blood volume (P less than 0.01), cardiac index (P less than 0.01), and heart rate (P less than 0.05). No significant differences were noted in stroke volume index or left ventricular dP/dt at 50 mmHg after prostaglandin E1. These results indicate that exogenously administered prostaglandin E1 causes active vasodilatation of the pulmonary vascular bed and has no inotropic action on the cardiac muscle.
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PMID:Effects of prostaglandin E1 on pulmonary circulation in patients with pulmonary hypertension. 73 98

The effect of prostaglandin E1 (PGE1) on central and peripheral hemodynamics was studied in seven conscious dogs under conditions of normoxia and hypobaric hypoxia to ascertain if hypoxia attenuated the cardiovascular actions of PGE1. Silastic catheters were chronically implanted in the pulmonary artery, left atrium, and aorta. Acute hypoxia was produced in a hypobaric chamber maintained at 446 mmHg pressure (14,000 feet). PGE1 at sea level (normoxia) resulted in significant increases in heart rate, cardiac output, left ventricular stroke work and pulmonary blood volume as well as significant decreases in aortic, pulmonary arterial, and left atrial pressures. During hypobaric hypoxia, PGE1 produced essentially identical effects on all hemodynamic parameters except pulmonary blood volume and pulmonary arterial pressure where marked attenuation of PGE1 action occurred.
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PMID:Effects of hypoxia on the hemodynamic actions of prostaglandin E1. 93 11

The effect of prostaglandin E1 on regional cerebral blood flow (rCBF) was studied with the intra-arterial 133Xe method in ten awake patients under local anesthesia. Measurements were taken from 16 areas of a hemisphere in seven patients, from 35 areas of a hemisphere in two patients and from 256 areas of a hemisphere in one patient. The prostaglandin was dissolved from the crystalline state without the aid of alcohol. It was given intracarotidly as a constant infusion at a rate of 5 ng per kilogram per minute for five minutes before the measurement and continued during the measurement. In every patient a mild increase in blood flow during the prostaglandin infusion was seen. The flow increase took place in all parts of the hemisphere. It averaged 11.2% (p less than 0.01). During the infusion, the skin supplied by the internal carotid artery and the conjunctiva on the infused side became red and sometimes swollen. A slight pressure was noted by most patients, but none had pain. No side effects of the infusion were noted.
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PMID:Effect of intracarotid prostaglandin E1 on regional cerebral blood flow in man. 100 30

The presence of an inotropic action of prostaglandin E1 (PGE1) in vivo is controversial, and there are conflicting results obtained by various indices of myocardial contractility. In this study, a direct effect of PGE1 on contractility was investigated in dogs by use of a load-independent contractile index: left ventricular end-systolic wall stress (LVESWS) versus the velocity of circumferential fiber shortening with rate-corrected (Vcfc) relationship using transesophageal echocardiography (TEE). Hemodynamics, arterial blood gas, and TEE data were obtained before PGE1 infusion (control), and with a 10%, 20%, and 30% decrease in mean arterial pressure (MAP) following intravenous PGE1 administration. PGE1 infusion rates were 0.19 +/- 0.03 at 10%, 0.82 +/- 0.17 at 20%, and 2.32 +/- 0.36 micrograms/kg/min at a 30% decrease in MAP. Pulmonary capillary wedge pressure, systemic vascular resistance index, and left ventricular stroke work index significantly decreased, and heart rate, cardiac index, and stroke volume index were not significantly altered. Analysis of the TEE data showed LVESWS (index of afterload) significantly decreased from 92.0 +/- 11.2 g/cm2 to 72.7 +/- 7.8 at 10%, 59.3 +/- 7.8 at 20%, and 44.6 +/- 6.2 at a 30% decrease in MAP, and Vcfc significantly increased from 0.595 +/- 0.065 circ/sec of control value to 0.670 +/- 0.056 at 10%, 0.824 +/- 0.049 at 20%, and 0.939 +/- 0.070 at a 30% decrease in MAP. In the LVESWS versus Vcfc relationship, no significant difference could be detected between the control state and the 10%, 20%, and 30% decrease in MAP, and no inotropic effect was found.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of prostaglandin E1 on myocardial contractility in dogs anesthetized with halothane: load-independent and noninvasive assessment using transesophageal echocardiography. 142 Oct 70

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

The effects of prostaglandin E1 (PGE1) on non-pulmonary vital organs in critically ill patients are not well defined. This study evaluated the role of exogenous PGE1 in systemic homeostasis during the adult respiratory distress syndrome (ARDS). Indicators of end-organ function were analyzed retrospectively in 146 septic or post-trauma patients with ARDS who received PGE1 (30/ng/kg/min) or placebo IV for up to 7 days in a randomized, double-blind clinical trial. Hemodynamic variables and serum levels of creatinine, bilirubin, and SGOT, platelet count, and changes in the white blood cell count were measured daily. Our results indicate that mean arterial pressure, pulmonary artery pressure, and systemic and pulmonary vascular resistance indices were significantly lower in the PGE1 group versus the placebo-treated group. Cardiac index, stroke index, and oxygen delivery index were significantly increased in the PGE1 group. Serum bilirubin and SGOT were decreased significantly among PGE1-treated patients compared with placebo-treated patients, while the white blood cell count increased more significantly from baseline values with PGE1 treatment. Intergroup differences in platelet count and serum creatinine levels were not statistically significant. The results indicate that PGE1 improves cardiovascular performance, hepatic function, and leukocyte availability during clinical ARDS. Prostaglandin E1 did not affect platelet counts and renal function in this study.
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PMID:The effects of prostaglandin E1 on non-pulmonary organ function during clinical acute respiratory failure. The Prostaglandin E1 Study Group. 156 22

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

The infusion of prostaglandin E1, a vasodilating substance with predominant effects on the pulmonary vasculature, has been found effective in the management of pulmonary hypertension associated with various diseases. The reported experience with prostaglandin E1 after cardiac transplantation is, however, limited. We used prostaglandin E1 in 18 patients in whom acute right ventricular failure developed after orthotopic cardiac transplantation. The infusion was started within 24 hours after operation in 16 patients and was continued for up to 7 days. Maximal doses of prostaglandin E1, administered via a central venous catheter, ranged from 30 to 120 ng/kg/min. Norepinephrine was simultaneously infused via a left atrial catheter in 10 patients to prevent a reduction in systemic arterial pressure. The prostaglandin E1 infusion resulted in significant reductions in mean arterial pressure and pulmonary vascular resistance and simultaneous increases in cardiac index and stroke index. Mean arterial pressure was stable and left ventricular stroke work increased. The alveolar oxygen tension/forced inspiratory oxygen index tended to decrease during the infusion. Three patients died, two of right heart failure and one of multiple organ failure associated with cardiac allograft rejection. In patients in whom right ventricular failure associated with pulmonary hypertension develops after cardiac transplantation, prostaglandin E1, combined with norepinephrine whenever the arterial pressure declines, can effectively reduce pulmonary artery pressures and improve global cardiac function without compromising systemic perfusion.
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PMID:Prostaglandin E1 infusion for right ventricular failure after cardiac transplantation. 830 1

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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