Cardiac protection from the viewpoint of coronary endothelial function
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AbstractDuring open heart surgery including coronary artery bypass grafting (CABG) using cardiopulmonary bypass, the heart is usually arrested for precise intracardiac repair or coronary grafting. Ischemia-reperfusion injury is the major problem in open heart surgery; cardioplegia was initially designed to protect the myocardium from this injury. It is now well known that coronary circulation plays a key role in myocardial perfusion. Injury to the coronary circulationmay change the coronary resistance and therefore affect the coronary flow. The reduction of coronary flow may damage the myocardium perfusion that, in addition to the ischemia-reperfusion injury to the myocardium, may further damage themyocardial function.Due to the differences between the cardiac myocytes and vascular (endothelial and smooth muscle) cells in structure and function, cardioplegia may have an adverse effect on coronary circulation; this has drawn the attention of many researchers in the past few decades. In addition to the usual cardioplegic solutions, for organ transplantation, cardioplegic or organ preservation solutions are used to preserve the heart or other organs. The endothelium-smooth muscle interaction may also be changed during the preservation. This chapter will discussmyocardial protection from the point of view of the protection of the coronary endothelial function. Endothelium is critical in regulating vascular tone, and the endothelium-dependent relaxation is mediated by three different endothelium-derived relaxing factors (EDRFs) - nitric oxide (NO), prostacyclin (PGI2), and endothelium-derived hyperpolarizing factor (EDHF) (Fig. 7.1) [1-3]. There is a considerable body of research on the endothelial function during cardioplegic arrest in cardiac surgery. Although some studies have suggested the preservative effect of crystalloid cardioplegic or organ preservation solutions on the endothelial function [4-6], numerous studies have provided evidence for endothelial damage after exposure to these solutions. Histological examination and cell culture approach also revealed that crystalloid hyperkalemic cardioplegic solutions impair the vascular endothelium and reduce the ability of coronary endothelial cells to replicate [7, 8]. © Springer-Verlag Berlin Heidelberg 2006.
All Author(s) ListYang Q., Yim A.P.C., He G.-W.
Pages63 - 70
LanguagesEnglish-United Kingdom

Last updated on 2020-01-08 at 02:41