Endothelial cell injury in cardiovascular surgery: the pathophysiology of vasomotor dysfunction

Abstract

Impaired vasomotor function has been suggested as playing a role in the pathophysiology of hypertension, diabetes, hypercholesterolemia, and atherosclerosis, all of which are common in cardiovascular surgery patients. In addition to chronic vasomotor dysfunction, alterations in vasomotor tone can result in acute arterial spasm, microcirculatory ischemia, and wide variations in systemic blood pressure. Changes in the health of the vascular endothelium may also impact the late patency of coronary artery bypass grafts, the progression of atherosclerosis in the native coronary circulation, and the long-term success of cardiac transplants. In the resting state the endothelium produces several substances that promote vascular relaxation and inhibition of platelet function, thus assuring the unhindered flow of blood through the capillaries. In response to injury, the endothelium loses some capacity to relax and also releases powerful vasoconstrictive agents. Attempting to understand the contributions that these substances play in the vasomotor dysfunction seen after cardiothoracic surgery is an area of active investigation.