Endothelial, platelet and leukocyte interactions in ischemic heart disease: Insights into potential mechanisms and their clinical relevance

Abstract

Recent investigations of the complex interactions among vascular endothelium, platelets and leukocytes have relevance to the pathogenesis of atherosclerosis and ischemic heart disease. Perturbations in the hemodynamic equilibrium maintained by these cellular elements may lead to vasospasm, in vivo thrombosis and a reduction in blood flow. Recent advances in the understanding of these interactions in health and disease states are summarized. The effect of pharmacologic agents on these cell-cell interactions are discussed to provide the reader with a general understanding of the relevance of these interactions in cardiovascular disease.

Association of white blood cell count with systolic blood pressure within the normotensive range

“…41 Stimulated granulocytes may have altered rheological properties with an increased tendency to adhere to vascular endothelium resulting in capillary leucostasis and subsequent increased vascular resistance. 42,43 Moreover, stimulated leucocytes release eicosanoids, platelet-activating factor and oxygenderived free radicals, which may initiate platelet aggregation 44 and release of potent vasoconstrictors serotonin and thromboxane A2; 45 this may produce microvascular obstruction by thrombus formation. An elevated WBC count may also be a marker for a state characterized by increased catecholamine levels or sympathetic nervous system activity, 16 which can raise blood pressure and may eventually result in sustained hypertension.…”

Fibrin(ogen)olytic and antiplatelet activities of a subtilisin-like protease from Solanum tuberosum (StSBTc-3)

“…Platelets readily aggregate in response to a variety of endogenous signals and secrete various compounds that cause further aggregation; they can initiate thrombus formation and precipitate thromboembolism, leading to ischemic diseases [48,49]. Antiplatelet activity has been reported for several plant proteases and plant extracts [16,50,51].…”

Sevoflurane reduces endothelium-dependent vasorelaxation: role of Superoxide anion and endothelin

“…However, a recent study has shown the inability of sevoflurane to interact chemically with NO and its ability to inhibit NO production directly in endothelial cells. 27 The originality of our study lies in the demonstration of the involvement of ET-1 in sevofluraneinduced endothelial dysfunction. Blockade of ETA-receptors by BQ-123 completely reverted the impaired vasorelaxing response to Ach in sevofluranetreated aortic segments.…”