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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Perinatal cerebral infarction, or stroke, is a not uncommon finding in newborns who survive after intensive care. Asphyxia, with its component parts hypoxemia and hypotension, represents the most common cause of perinatal cerebral infarction and may result in neuropathological changes in the periventricular white matter. Previous studies have demonstrated regional alterations in cerebral blood flow (CBF) in response to hypoxemic insult. This work examines the effects of hypoxemia on regional cerebral prostaglandin levels in the developing brain, since some observers believe that local CBF is controlled in part by prostaglandins. In this study, newborn beagle pups were anesthetized, subjected to tracheotomy and artificially ventilated to maintain normoxemia and normocarbia. Mean arterial blood pressure (MABP) was continuously monitored by means of an indwelling catheter and transducer, and craniectomies were performed. When the pups were physiologically stabilized, they were randomly assigned to receive acute hypoxemic insult (pO2 14.0 +/- 1.55 mm Hg, mean +/- standard deviation) accomplished by altering the oxygen concentration in the inspired air) or to receive no insult (mean pO2 84.3 +/- 13.0 mm Hg). Fifteen minutes following stable hypoxemic or normoxic conditions, all pups underwent in vivo freezing of the intracranial contents under anesthesia followed by rapid sacrifice. No significant differences were noted between the MABP, pH, or pCO2 values for the control and hypoxemic pups during the experimental period. Regional cerebral prostaglandin data demonstrated a significant increase in prostaglandin (PG)E2 in the gray matter of hypoxemic pups when compared to the normoxic controls (p less than 0.02). No significant differences were noted for 6-keto-PGE1 alpha, the stable metabolite of prostacyclin, or thromboxane (TX)B2, the stable metabolite of TXA2, in the gray matter. In addition, although 6-keto-PGE1 alpha was significantly lower in the periventricular white matter of the hypoxemic pups (p less than 0.05), there were no changes in the white matter in either PGE2 or TXA2. This regional differential synthesis of PGE2 in response to hypoxemic insult may explain the relative failure of CBF to the periventricular white matter and thus the neuropathological alterations attributed to it.
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PMID:Beagle puppy model of perinatal cerebral infarction. Regional cerebral prostaglandin changes during acute hypoxemia. 377 84

Fourteen patients with acute myocardial infarction (duration of chest pain 5 +/- 2 hours) received intracoronary infusion of prostaglandin E1 (PGE1) and streptokinase. Intracoronary PGE1 was followed by intracoronary streptokinase in 10 patients (group A), with successful recanalization in all patients. Of 4 patients in whom recanalization failed with intracoronary streptokinase given first (group B), 2 had successful recanalization after addition of intracoronary PGE1. Immediately after successful recanalization, left ventricular ejection fraction increased from 50 +/- 9% to 62 +/- 10% (p less than 0.0008), left ventricular end-diastolic pressure decreased from 20 +/- 10 to 16 +/- 10 mm Hg (p less than 0.05) and stroke volume index increased from 34 +/- 10 to 44 +/- 12 ml/m2 (p less than 0.02). Infarct segment shortening improved from 9 +/- 5 to 18 +/- 4% (p less than 0.0002). Transient hypotension in 1 patient was the only complication. Follow-up catheterization in recanalized patients at 2 to 10 days showed maintained improvement in left ventricular global and infarct segment function. Reocclusion occurred in 1 patient. Thus, intracoronary infusion of PGE1 was effective in establishing reperfusion in all patients when followed by streptokinase and was associated with immediately improved left ventricular global and regional function. PGE1 deserves further evaluation in acute myocardial infarction.
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PMID:Intracoronary prostaglandin E1 plus streptokinase in acute myocardial infarction. 378 2

The hemolysate (10(-5)-10(-2) times dilution; original hemoglobin concentration was 0.83 +/- 0.10 X 10(-3)M) evoked the contraction in a dose dependent manner, and this contraction was composed of low and high sensitive responses as estimated from the Eadie-Hofstee's plot. Indomethacin (10(-7)-10(-5)M) inhibited the latter component in the hemolysate-induced contraction. The membrane potential of smooth muscle cells was -50 mV and the cell was electrically quiescent. The hemolysate (greater than 10(-2) times dilution) depolarized the membrane and increased the ionic conductance of membrane. In rare occasions, the spike potential was triggered on the hemolysate-induced depolarization. The hemolysate (10(-5)-3 X 10(-3) times dilution) produced the contraction with no change in the membrane property. Carbocyclic thromboxane A2 ( cTXA2 ; 2.8 X 10(-10)M) produced the contraction without depolarization of the membrane, yet the TXA2 synthesis inhibitor, OKY-1581 (10(-5)M), had no effect on the hemolysate-induced contraction. PGE1, PGE2 and PGF2 alpha (2.8 X 10(-6)M) produced the contraction with no change in the membrane property. The contraction evoked by 2.8 X 10(-6)M PGF2 alpha corresponded well with that evoked by 3 X 10(-3) times dilution of the hemolysate. Removal of the endothelium by mechanical rubbing modified the hemolysate-induced contraction. Under the assumption that OKY-1581 is a selective inhibitor for TXA2 synthesis, the major part of the contraction (the indomethacin sensitive component) of the basilar artery is postulated to be due to synthesis of the primary PG rather than TXA2 by the hemolysate, yet the hemolysate itself, has to some extent a direct action in evoking the small contraction.
Stroke
PMID:Hemolysate-induced contraction in smooth muscle cells of the guinea pig basilar artery. 672 80

We examined whether endogenous prostaglandins (PGs) participated in control of hindquarters vascular resistance during salt loading in stroke-prone spontaneously hypertensive rates (SHR-SP). SHR-SP and Wistar-Kyoto rats (WKY) were fed either a normal (0.3% NaCl) or high (8% NaCl) salt diet for 5 wk. High salt increased blood pressure and hindquarter vascular resistance (VR) in SHR-SP (P less than 0.01) but not in WKY. Indomethacin given intravenously increased hindquarter VR in SHR-SP during high salt as well as during normal salt (P less than 0.01) but not in either group of WKY. In SHR-SP the increase in hindquarter VR by PG synthesis inhibitors were two times greater during high salt than during normal salt (P less than 0.01). In addition, hindquarter vasodilatation by bradykinin was greater (P less than 0.05) in SHR-SP during high salt than that during normal salt, but vasodilatation by prostaglandin E1 or nitroglycerin was not different between the two groups. These results suggest that vascular synthesis of endogenous PGs was greater in SHR-SP during high salt than that during normal salt. Increased endogenous PGs may play an important role in the regulation of hindquarter VR during high salt intake in SHR-SP.
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PMID:Salt loading augments vascular responses to indomethacin in stroke-prone SHR. 681 Jul 12

Although one-hour infusions of prostaglandin E1 to animals suffering from hemorrhagic shock have proved beneficial, there is question as to whether the improved hemodynamics can be sustained over a longer infusion time. Following reinfusion of shed blood, an infusion of PGE1 at a dose of 1 microgram/kg/minute showed a significant elevation in cardiac output and left ventricular stroke work and a decrease in systemic vascular resistance when compared to animals receiving only an equal volume of normal saline. There was no diminution in the hemodynamic activity of the drug over the entire infusion period. These data indicate that the drug might be appropriate for hemodynamic support in the clinical situation, where infusion times of greater than one hour are often necessary.
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PMID:Hemodynamic effects of prolonged infusion of prostaglandin E1 (PGE1) after hemorrhagic shock. 689 Mar 4

To provide more effective vasodilator agents for the therapy of severe left ventricular (LV) failure the cardiocirculatory actions of prostaglandin E1 (PGE1) were evaluated in nine coronary patients. PGE1 infusion modestly decreased mean systemic blood pressure (85 to 76 mm Hg, p less than 0.025) and LV filling pressure (19 to 15 mm Hg, p less than 0.01) while heart rate was unchanged (p less than 0.05). Simultaneously, PGE1 augmented cardiac index from 1.9 to 2.5 1/min/m2 (p less than 0.005), raised stroke index from 28 to 35 ml/beat m2 (p less than 0.01) and increased stroke work index from 26 to 30 g-m/m2 (p less than 0.02). Additionally, total systemic vascular resistance decreased from 1862 to 1282 dynes-sec-cm-5 (p less than 0.02) and double product of heart rate and systolic blood pressure diminished from 9492 to 8278 mm Hg (p less than 0.02) while the effective endocardial perfusion pressure was maintained (p less than 0.05). Concomitantly, forearm vascular resistance fell, forearm blood flow was raised, and forearm venous tone remained unchanged. Thus, our results demonstrate that PGE2 is a potent arteriolar vasodilator with markedly beneficial effects of myocardial energetics and on cardiac function in patients with severe ischemic congestive cardiac failure.
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PMID:Beneficial effects of prostaglandin E1 on myocardial energetics and pump performance in severe CHF. 694 63

The hemodynamic effect of prostaglandin E1 (PGE1) on acute respiratory failure is investigated. Eight adult mongrel dogs were subjected to oleic acid-induced acute respiratory failure. Four dogs received PGE1 intravenously one hour after oleic acid injection, and four received an equal volume of saline. Cardiac output, arterial PO2 and alveolar-arterial oxygen difference decreased significantly in the saline-treated animals, and systemic vascular resistance increased. These parameters were maintained in the PGE1 group, and stroke volume and arterial-venous oxygen difference were improved. Pulmonary vascular resistance increased in both groups. This beneficial effect of PGE1 in acute respiratory failure may be related to maintenance of hemodynamics and pulmonary gas exchange and to improved tissue oxygenation.
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PMID:The hemodynamic effects of prostaglandin E1 (PGE1) in acute hypoxic respiratory failure. 719 70

Prostaglandin E1 (PGE1) has been shown to limit infarct size, improve coronary blood flow, inhibit platelet aggregation, and reduce both left ventricular (LV) preload and afterload in experimental animals. Its use in the therapy of patients with acute myocardial infarction (AMI) and congestive heart failure (CHF) has not, however, been reported. Five patients with AMI of less than 12 hours' duration and LV dysfunction were studied to assess the hemodynamic effects of IV infusion of PGE1. PGE1 in the concentration of 0.4 microgram/ml was infused at a rate of 0.003 microgram2kg/min (3 ng . kg-1 . min-1) to a maximum rate of 0.021 microgram/kg/min (21 ng . kg-1 . min-1) for a total time of up to 90 minutes. There was an insignificant increase in heart rate, with significant decreases in mean arterial blood pressure and systemic vascular resistance. Pulmonary capillary wedge pressure declined from 21 +/- 3 to 15 +/ 1 mm Hg (p less than 0.05), mean pulmonary artery pressure and pulmonary vascular resistance decreased (p less than 0.05), mean pulmonary artery pressure and pulmonary vascular resistance decreased (p less than 0.05), with increases in cardiac index from 2.38 +/- 0.08 to 2.89 +/- 0.58 L/min/m2 (p less than 0.01) and stroke volume from 51 +/- 17 to 59 +/- 20 ml/beat (p less than 0.05). No major cardiac or extracardiac side effects were encountered during PGE1 infusion. One patient had transient nausea which did not require discontinuation of the drug. PGE1 is an effective vasodilator and deserves further application in therapy for AMI patients with CHF.
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PMID:Hemodynamic effects of prostaglandin E1 infusion in patients with acute myocardial infarction and left ventricular failure. 719 15

The cardiocirculatory actions of brief (69 +/- 5 minutes) infusions of prostaglandin E1 were evaluated in nine chronic coronary heart disease patients with severe left ventricular (LV) failure caused by previous myocardial infarction. Prostaglandin E1 infusion did not alter heart rate (HR) and produced modest declines in mean systemic blood pressure (BP) (85 +/- 6 to 76 +/- 5 mm Hg, P less than 0.025) and LV filling pressure (19 +/- 3 to 15 +/- 2 mm Hg, P less than 0.01). Simultaneously, prostaglandin E1 augmented LV pump function raising cardiac index from 1.9 +/- 0.2 to 2.5 +/- 0.1 L/min/m2 (p less than 0.005), elevating stroke index from 28 +/- 2.4 to 35 +/- 2.9 ml/beat/m2 (p less than 0.01), and increasing stroke work index from 26 +/- 4.3 to 30 +/- 4.4 gm . m/m2 (p less than 0.02). Additionally, total systemic vascular resistance decreased from 1862 +/- 192 to 1282 +/- 100 dynes-sec-cm-5 (p less than 0.02) and double product LV aerobic index of HR . systolic BP diminished from 9492 +/- 666 to 8278 +/- 492 (p less than 0.02). Concomitantly, in the forearm, vascular resistance fell, blood flow rose, and venous tone remained unchanged. These results indicate that prostaglandin E1 is a potent systemic arteriolar dilator with markedly beneficial effects on cardiac function in chronic coronary patients having severe ischemic LV failure refractory to conventional therapy.
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PMID:Cardiocirculatory and myocardial energetic effects of prostaglandin E1 in severe left ventricular failure due to chronic coronary heart disease. 728 15

Cardiac output, heart rate, stroke volume, pressures in the brachial artery, right ventricle and pulmonary artery, forearm blood flow, and arterial concentration of FFA, lactate and glucose were measured in healthy male volunteers during i-v infusion of PGE1, PGE2, PGF2 alpha or 15-methyl PGF2 alpha in increasing doses. In accordance with previous findings PGE1 and PGE2 increased cardiac output by a vasodilating effect in the systemic and pulmonary vascular bed, probably in combination with an inotropic effect on the heart. 15-methyl PGF2 alpha had essentially the same cardiovascular effects as PGF2 alpha. They induced a slight increase in cardiac output due to effects on heart rate, while systemic vascular resistance was unchanged. Forearm vascular resistance increased and pressures in the pulmonary circulation rose, indicating a vasoconstriction in these vascular beds. Glucose concentrations was not affected nor were lactate concentrations, except for a slight decrease of unclear significance in the group receiving 15-methyl PGF2 alpha. FFA increased slowly in the same manner as seen spontaneously in fasting individuals. These data do not indicate direct metabolic effects of the prostaglandins studied when given i-v.
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PMID:Central and peripheral circulatory effects and metabolic effects of different prostaglandins given I.V. to man. 741 95


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