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CORONARY ENDOTHELIAL FUNCTION IN OPEN HEART SURGERY
Author(s) -
He GuoWei
Publication year - 1997
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1997.tb02726.x
Subject(s) - bradykinin , endothelium , hyperpolarization (physics) , medicine , cardiology , calcium , contraction (grammar) , calcium in biology , endothelial stem cell , depolarization , anesthesia , chemistry , endocrinology , biochemistry , receptor , organic chemistry , nuclear magnetic resonance spectroscopy , in vitro
SUMMARY 1. During open heart surgery, the heart is arrested and protected by hyperkalaemic cardioplegia. The coronary endothelium may be damaged by ischaemia‐reperfusion and cardioplegia. Subsequently, this may affect cardiac function immediately after cardiac surgery and cause mortality or morbidity. 2. Our studies have investigated coronary endothelial function after exposure to hyperkalemi. (K + 20 or 50 mmol/L). Endothelium‐dependent relaxation and hyperpolarization of the coronary smooth muscle and intracellular free calcium concentration in the endothelial cell were measured with regard to K + exposure. 3. Endothelium‐derived hyperpolarizing factor (EDHF)‐mediated relaxation to A23187, bradykinin, and substance P in the presence of either U46619 (10 nmol/L)‐ o. K + (25 mmol/L)‐induced contraction was reduced after exposure to either 20 or 50mmol/LK. + 4. The hyperpolarization of the membrane potential in response to the endothelium‐derived relaxing factor (EDRF) stimuli was also reduced by exposure t. K + . 5. The intracellular free calcium concentration remained unchanged after exposure t. hyperkalemia. 6. We conclude that the EDHF‐mediated coronary endothelial function is impaired after exposure to hyperkalaemic cardioplegia. The impairment of this function is due to the changed effect of EDHF on the smooth muscle cell, probably through partially depolarizing the membrane and affecting K + channels rather than alteration of its biosynthesis/release in the endothelial cell. It may be of use to search for a new cardioplegia that preserves this endothelial function during open heart surgery.