Table of Contents
ISRN Physiology
Volume 2013, Article ID 238979, 24 pages
Review Article

The Coronary Microcirculation in Health and Disease

Department of Physiology and Functional Genomics, University of Florida College of Medicine, P.O. Box 100274, Gainesville, FL 32610-0274, USA

Received 15 May 2013; Accepted 6 June 2013

Academic Editors: I. Bernatova and A. V. Zholos

Copyright © 2013 Judy M. Muller-Delp. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Coronary blood flow is closely regulated to meet the changing metabolic demands of the working myocardium. Resistance of the coronary vasculature is determined by metabolic, myogenic, endothelial, and neural mechanisms. The influence of these control mechanisms varies throughout the coronary circulation, as they have dominant sites of action in vessels of different caliber. Coronary vascular resistance depends upon the coordinated response to these influences. Within a segment of the coronary circulation, resistance may be determined, for example, by competitive interaction between neural vasoconstriction and metabolic vasodilation. Such a system in which control occurs through multiple mechanisms with varying effects allows for precise control of coronary blood flow. This system also provides protection against dysfunction of a single control mechanism. If one fails, other control mechanisms can compensate for that loss of function. Thus, adequate delivery of oxygen and nutrients can be maintained despite potential dysfunction and large fluctuations in metabolic demands of the myocardium. In disease states, these regulatory mechanisms may also fail, and endothelial dysfunction is commonly seen in the setting of cardiac disease. Optimal cardioprotective therapies must target the coronary microcirculation and cardiac myocytes in tandem. Similarly, reversal of cardiac dysfunction requires concomitant amelioration of coronary microvascular dysfunction.