Journal ArticleDOI
Studies on the protective effect of prostacyclin in acute myocardial ischemia
Martin L. Ogletree,Martin L. Ogletree,Allan M. Lefer,Allan M. Lefer,J. Bryan Smith,J. Bryan Smith,Kyriacos C. Nicolaou,Kyriacos C. Nicolaou +7 more
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TLDR
PGI2 infusion may protect the ischemic myocardium by reducing oxygen demand, primarily through reductions in cardiac work, and by perhaps inhibiting platelet aggregation and preserving myocardial cell integrity.About:
This article is published in European Journal of Pharmacology.The article was published on 1979-06-01. It has received 150 citations till now. The article focuses on the topics: Ischemia & CATS.read more
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A randomized controlled trial of epoprostenol therapy for severe congestive heart failure: The Flolan International Randomized Survival Trial (FIRST)
Robert M. Califf,Kirkwood F. Adams,William J. McKenna,Mihai Gheorghiade,Barry F. Uretsky,Steven McNulty,Harald Darius,Kevin A. Schulman,Faiez Zannad,Eileen Handberg-Thurmond,Frank E. Harrell,William S. Wheeler,Jordi Soler-Soler,Karl Swedberg +13 more
TL;DR: In this paper, the authors evaluated the effects of epoprostenol on patients with severe left ventricular failure and found that the median dose was 4.0 ng/kg/min, resulting in a significant increase in cardiac index (1.81 to 2.61 L/min/m 2 ).
Journal ArticleDOI
Cardiovascular effects of exercise: Role of endothelial shear stress
Josef Niebauer,John P. Cooke +1 more
TL;DR: The underlying mechanisms by which exercise-induced blood flow and shear stress exert their salutary effects on cardiovascular remodeling are discussed.
Journal ArticleDOI
Free radicals and myocardial ischemia and reperfusion injury
TL;DR: The current understanding of the events associated with myocardial ischemia suggests that within the ischemicMyocardial region or area at risk, there is a population of cells that are reversibly injured and that reperfusion within a specified period (less than 3 hours) of time is capable of restoring the majority of the jeopardized cells to a normal status, but that the act of reperfusions itself will lead to the sudden demise of a fraction of the cells.
Journal ArticleDOI
Pharmacology of the Endothelium in Ischemia-Reperfusion and Circulatory Shock
Allan M. Lefer,David J. Lefer +1 more
TL;DR: Endothelial dysfunction is an important early-recurring phenomenon in virtually all forms of ischemia-reperfusion, including a variety of circulatory shock states and may be amplified by neutrophil-generated factors including oxygen-derived free radicals, cytokines, proteases, and lipid mediators.
Journal ArticleDOI
Pharmacodynamic profile of prostacyclin
John R. Vane,Regina M. Botting +1 more
TL;DR: Prostacyclin is the main product of arachidonic acid in all vascular tissues tested to date and strongly vasodilates all vascular beds studied, and is the most potent endogenous inhibitor of platelet aggregation yet discovered.
References
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Determination of serum proteins by means of the biuret reaction.
TL;DR: An investigation of the biochemical changes following experimental liver injury felt the need of a simple, rapid, and accurate method for determining the protein fractions in small amounts of serum and began with Kingsley’s biuret procedure.
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Aggregation of blood platelets by adenosine diphosphate and its reversal.
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An enzyme isolated from arteries transforms prostaglandin endoperoxides to an unstable substance that inhibits platelet aggregation.
TL;DR: A balance between formation of anti- and pro-aggregatory substances by enzymes could also contribute to the maintenance of the integrity of vascular endothelium and explain the mechanism of formation of intra-arterial thrombi in certain physiopathological conditions.
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An improved procedure for serum creatine phosphokinase determination.
TL;DR: The creatine phosphokinase activity of serum is determined by a procedure in which adenosine triphosphate, liberated by the action of the enzyme, is linked to the reduction of nicotinamide-adenine dinucleotide phosphate and the formation of reduced nicotinamides followed spectrophotometricically.
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Arterial walls are protected against deposition of platelet thrombi by a substance (prostaglandin X) which they make from prostaglandin endoperoxides
TL;DR: It is concluded that a balance between formation by arterial walls of PGX which prevents platelet aggregation and release by blood platelets of prostaglandin endoperoxides which induce aggregation is of the utmost importance for the control of thrombus formation in vessels.