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Vascular Endothelial Function Related to Cardiac Surgery

Hong Kong, China

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Vascular endothelium has multiple functions including regulating vascular tone, preventing platelet aggregation, anti-proliferation etc. All these functions are important in physiological and pathophysiological status. The regulation of vascular tone – the endothelium-dependent relaxation is mediated by three endothelium-derived relaxing factors¹ (EDRFs) – nitric oxide (NO), prostacyclin (PGI₂), and an unidentified endothelium-derived hyperpolarizing factor (EDHF).

PGI₂ is the first defined relaxing factor derived from endothelium and it is converted from arachidonic acid (AA) by cyclooxygenase (COX). PGI₂ causes vasorelaxation in most arteries, including the coronary bed by increase of cyclic 3', 5'-adenosine monophosphate (cAMP). Different types of potassium (K⁺) channels are also involved.

NO is synthesized from the amino acid L-arginine by NO synthase (NOS). There are at least two major NOS isoforms: 1) cNOS is expressed constitutively in neurons and vasculature that is involved in cell communication and is activated by an increase in intracellular calcium. 2) iNOS exists in macrophages to participate in host defense and is not normally found in endothelial cells or vascular smooth muscle unless induced by cytokines. NO induces vasorelaxation through cyclic 3', 5'-guanosine monophosphate (cGMP) mechanism.² Several types of K⁺ channels are also involved in NO-mediated hyperpolarization.

The endothelium-dependent hyperpolarization and relaxation are only partially inhibited or not changed with the presence of COX and NOS inhibitors, indicating the existence of a novel vasorelaxant agent named EDHF, which is distinct from PGI₂ and NO.^3,4 Several substances have been suggested to be EDHF, such as epoxyeicosatrienoic acid (EETs), anadamide, . . . [Full Text of this Article]

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