Abstract

The assumption that the coronary capillary blood flow is exclusively regulated by precapillary vessels is not supported by recent data. Rather, the complex coronary capillary bed has unique structural and geometric characteristics that invalidate many assumptions regarding red blood cell (RBC) transport, for example, data based on a single capillary or that increases in flow are the result of capillary recruitment. It is now recognized that all coronary capillaries are open and that their variations in flow are due to structural differences, local O2 demand and delivery, and variations in hematocrit. Recent data reveal that local mechanisms within the capillary bed regulate flow via signaling mechanisms involving RBC signaling and endothelial-associated pericytes that contract and relax in response to humoral and neural signaling. The discovery that pericytes respond to vasoactive signals (e.g., nitric oxide, phenylephrine, and adenosine) underscores the role of these cells in regulating capillary diameter and consequently RBC flux and oxygen delivery. RBCs also affect blood flow by sensing and releasing nitric oxide to facilitate relaxation of pericytes and a consequential capillary dilation. New data indicate that these signaling mechanisms allow control of blood flow in specific coronary capillaries according to their oxygen requirements. In conclusion, mechanisms in the coronary capillary bed facilitate RBC density and transit time, hematocrit, blood flow and O2 delivery, factors that decrease capillary heterogeneity. These findings have important clinical implications for myocardial ischemia and infarction, as well as other vascular diseases.

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