0000000000292789

AUTHOR

Uwe M. Fischer

Pneumocyte Apoptosis Induction during Cardiopulmonary Bypass: Effective Prevention by Radical Scavenging UsingN-Acetylcysteine

Cardiopulmonary bypass (CPB) and cardioplegic arrest are associated with pulmonary dysfunction. We sought to investigate whether pulmonary ischemia/reperfusion during standard CPB and cardioplegic arrest is associated with reactive oxygen species (ROS)-mediated pulmonary tissue injury and pneumocyte apoptosis induction, and whether ROS scavenging using N-acetylcysteine (NAC) attenuates these alterations. Twelve pigs (41 +/- 8 kg) were randomized to receive either NAC (100 mg/kg prior to CPB; n = 7) or placebo (n = 5) and subjected to CPB and 60 min of cold (4 degrees C) crystalloid cardioplegic arrest. We collected lung biopsies prior to CPB, at 60 min CPB, as well as at 30, 60, and 120 min…

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Regulation of endothelial nitric oxide synthase (eNOS) in myocardium subjected to cardioplegic arrest.

BACKGROUND: Nitric oxide (NO) production by both coronary endothelial cells and cardiomyocytes is thought to play a significant role in myocardial pathophysiology following ischemia/reperfusion (I/R). METHODS: In thirteen pigs subjected to 1 hour cardioplegic arrest (CA) on CPB, left ventricular (LV) biopsies were collected prior to CPB (baseline), at 60 min CPA, at 15 and 30 min reperfusion on CPB, and at 120 min post CPB. LV specimens were immunocytochemically stained against phospho-eNOS Ser1177 , phospho-eNOS Thr495 , phosphorylated ERK1/2, and AKT/PKB. Four additional pigs without CA served as controls. Cardiomyocytes were quantitatively investigated using TV densitometry (gray units: …

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Extracorporeal circulation activates endothelial nitric oxide synthase in erythrocytes.

Background Extracorporeal circulation used in cardiopulmonary bypass and hemodialysis is often associated with severe hypotension, which is an important predictor for mortality and morbidity. One pathophysiological hypothesis includes nitric oxide (NO) generation. Recently, a functional NO synthase (endothelial type NO synthase [eNOS]), was found to be expressed in human red blood cells. However, to date, activation of red blood cell eNOS has not been shown. We hypothesized that eNOS in circulating red blood cells might be activated during extracorporeal circulation and thus contribute to hypotension through vasodilation upon NO release. Methods We collected blood samples from 28 patients e…

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