Preservation of the Endothelium in Cardiovascular Surgery – Some Practical Suggestions – A review

Abstract

The most vulnerable structure in vascular tissue is the endothelium, which plays a critical role in the maintenance of normal vessel wall structure and function. Endothelial cells produce a variety of biologically active substances which control vascular permeability, vessel tone, coagulation, Ž brinolysis and in ammatory responses. Some of these substances, such as the proteins of cellular junctions or adhesion molecules, are integral parts of the cell structure whereas others, such as nitric oxide (NO), prostacyclin, chemokines, or factors involved in coagulation and Ž brinolysis, are produced and then released by endothelial cells either luminally or abluminally (1). The endothelium is antithrombogenic when well preserved, and yet promotes platelet aggregation and coagulation if injured. Vasospasm, occlusive intimal hyperplasia and accelerated atherosclerosis can also all occur as a result of bad endothelial preservation (2). The persons who are faced most directly with the problems of endothelial preservation in cardiovascular surgery are the surgeons transplanting hearts and lungs; if the endothelium is badly preserved in the donor organ, the blood cells of the recipient may not be able to pass through the capillaries due to endothelial swelling, and multiple infarctions and death of the recipient may occur. In most published data on heart and lung transplantation, the early mortality due to “primary organ failure” is in the range of 10–25%, attesting to the signiŽ cance of the problem. Coronary surgeons are also transplantation surgeons: they harvest blood vessel segments, veins or arteries, and transplant them into the coronary circulation. Although this is autotransplantation, it is still transplantation, and the complex and vulnerable vascular tissue they transplant should be preserved using the same principles as those used by transplant surgeons in general. During prolonged cardiopulmonary bypass (CPB), the lungs may suffer ischemic injury and the use of cold crystalloid cardioplegia delivered under high pressure into the coronary arteries may elicit endothelial injury, initiating vasospasm and accelerated atherosclerosis. This review article will give some practical suggestions on how to minimize these problems. Once every minute the entire blood volume passes through the pulmonary artery, which could be compared with a big vascular tree, branching out to meet the air in the alveolocapillary membrane, making possible the vital gas exchange of the blood. During CPB blood still  ows in the pulmonary circulation, coming from the bronchial arteries, but it is important to keep in mind in these days of “warm heart surgery” (3), that the bronchial circulation alone cannot supply the lungs with enough blood during normothermia to prevent ischemic lung injury (4, 5). If the bypass time for unexpected reasons needs to be prolonged, cooling or pulmonary artery perfusion should be initiated. The young cardiac surgeon should never forget that the golden standard temperature used for many years during CPB was 28°C, and that many senior surgeons even today cool their patients routinely to at least 32°C during CPB. In pigs, at least 25% of the cardiac output must be directed through the pulmonary artery at normothermia to prevent ischemic lung injury (5). If the cardiac output can be directed through the pulmonary artery, total extracorporeal membrane oxygenation (veno-right ventricular ECMO) supplying a patient’s whole need for gas exchange, can be run for several weeks without causing lung injury (6–8). However, total veno-arterial ECMO, bypassing the pulmonary artery circulation, cannot be run for more than a few hours before ischemic injury of the lung vasculature occurs, manifesting itself after weaning from bypass as increased pulmonary vascular resistance or intrapulmonary bleeding (4, 5). In lung transplantation, preservation of the donor lungs has until recently been obtained by cold  ush perfusion of the pulmonary artery with Euro-Collins solution, a high-potassium kidney preservation solution developed in the 1960s. For preservation of vascular tissue, Euro-Collins solution is inferior to Perfadex (9), a low-potassium dextran (LPD) solution, also developed in the 1960s as a kidney preservation solution. Perfadex gives excellent lung (10) and vascular (9, 11) preservation for 24 h. By switching over from EuroCollins to Perfadex in clinical lung transplantation,