Blood cardioplegia enhanced with nitric oxide donor SPM-5185 counteracts postischemic endothelial and ventricular dysfunction
- 30 June 1995
- journal article
- research article
- Published by Elsevier in The Journal of Thoracic and Cardiovascular Surgery
- Vol. 109 (6) , 1146-1154
- https://doi.org/10.1016/s0022-5223(95)70198-2
Abstract
No abstract availableKeywords
This publication has 28 references indexed in Scilit:
- Coronary artery endothelial dysfunction after global ischemia, blood cardioplegia, and reperfusionThe Annals of Thoracic Surgery, 1994
- Global myocardial ischemia and reperfusion impair endothelium-dependent relaxations to aggregating platelets in the canine coronary arteryThe Journal of Thoracic and Cardiovascular Surgery, 1992
- Nitric oxide: an endogenous modulator of leukocyte adhesion.Proceedings of the National Academy of Sciences, 1991
- Time course of endothelial dysfunction and myocardial injury during myocardial ischemia and reperfusion in the cat.Circulation, 1990
- Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factorNature, 1987
- Endothelium‐derived relaxing factor inhibits in vitro platelet aggregationBritish Journal of Pharmacology, 1987
- Reperfusion after acute coronary occlusion in dogs impairs endothelium-dependent relaxation to acetylcholine and augments contractile reactivity in vitro.Journal of Clinical Investigation, 1987
- Superoxide anion is involved in the breakdown of endothelium-derived vascular relaxing factorNature, 1986
- Oxygen-Derived Free Radicals in Postischemic Tissue InjuryNew England Journal of Medicine, 1985
- Coronary Vascular Reactivity After Acute Myocardial IschemiaScience, 1982