The microcirculation is particularly vulnerable to the pathologic effects of ischemia and reperfusion (I/R), with postischemic endothelial dysfunction occurring in all segments of the microvasculature and becoming evident as one of the earliest responses to reperfusion. For example, endothelium-dependent arteriolar vasoregulatory mechanisms are disrupted in postischemic tissues and contribute to the development of I/R-induced perfusion deficits in localized areas of ischemic tissues. Impaired arteriolar vasoregu-lation also appears to be a primary cause of variant angina and coronary vasospasm. The barrier function of endothelial cells in capillaries and postcapillary venules is also compromised as a consequence of I/R, an effect that leads to enhanced fluid and protein leakage from these vessels and the formation of interstitial edema. The accumulation of fluid in the extravascular compartment increases the path length over which oxygen must diffuse to reach parenchy-mal cells. This effect is exacerbated by postischemic endothelial cell swelling and edema-induced extravascular compression of the capillary lumen, processes that contribute to insufficient nutritive perfusion in I/R, a phenomenon referred to as capillary no-reflow. Postcapillary venular endothelium also participates in the production of I/R injury by coordinating the arrest and infiltration of leukocytes in ischemic regions, which then direct a focused attack upon parenchymal cells. I/R-induced platelet adhesion in postcapillary venules may facilitate this leukosequestration while their interactions with each other, leukocytes, and/or the arteriolar wall may promote thrombogenesis.
The aforementioned considerations indicate that preservation of endothelial function should be an important therapeutic goal in I/R. Of the many avenues pursued in this regard, preconditioning tissues to resist the deleterious effects of prolonged ischemia and reperfusion by antecedent exposure to ethanol represents one of the most promising interventions studied to date. For example, the effects of I/R to induce endothelial-dependent vasoregulatory dysfunction in arterioles, nutritive perfusion failure in capillaries (capillary no-reflow), adhesion molecule expression and leukocyte adherence in postcapillary venules, and endothelial barrier disruption in capillaries and postcapillary venules are completely prevented by prior ethanol ingestion. Of the beneficial actions microcirculatory actions that are induced by antecedent ethanol ingestion, our best mechanistic understanding pertains to its anti-inflammatory effects in postcap-illary venules. Thus, this effect will be reviewed in the more detail.
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