Background: Ischemic heart disease has long been considered to be exlusively caused by stenosis or occlusion. However, the coronary microcirculation too may play an important role in ischemic conditions. Also, the crucial role of microvessels in not only regulating blood flow on a local level but also mediating vascular permeability or inflammatory responses has been recognized.
Objective: To review important physiological and pathophysiological mechanisms of coronary microcirculatory control with focus on heterogeneity of local perfusion, microvascular permeability and inflammation.
Method: Selective research of the literature.
Results: Heterogeneity is a characteristic of microvascular networks and affects structural and functional parameters such as vessel diameter, length, and connection pattern, flow velocity, wall shear stress, and oxygenation. Microvascular networks are optimized to meet the metabolic demand of all tissue compartments. This requires continuous vascular adaptation regulated by local hemodynamic and metabolic stimuli. Compromising this regulation results in functional arterio-venous shunting and tissue areas with either hyperperfusion or hypoxia in close proximity. In ischemia-reperfusion, increased microvascular permeability may aggravate tissue hypoxia by increasing extravascular pressure and seems to contribute to adverse myocardial remodeling. Transendothelial transport mechanisms and deterioration of the endothelial glycocalyx seem to be major contributors to tissue edema. Also in the context of ischemia-reperfusion, an inflammatory response mediated by venular endothelium expressing specific adhesion molecules contributes to tissue injury. However, anti-inflammatory therapies failed in clinical studies and a multi-targeted approach for cardiac protection is required.
Conclusion: Disturbances of the coronary microcirculation are involved in different pathophysiological aspects of reperfusion injury.
Keywords: Microvessels, heterogeneity, angioadaptation, vascular permeability, inflammation, leucocyte-endothelium interaction.
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