Mechanisms of Increased Tissue Oxygen Delivery Following Release of Arterial Occlusion in Canine Skeletal Muscle and Skin

Abstract

Tissue oxygen delivery is dependent on the local blood flow and the extent of oxygen extraction. Concerning the intrinsic microvascular control of tissue O₂ delivery, a recent system analysis (1) and experimental data (2) suggest that adequate tissue oxygenation is maintained over a wide range of metabolic stresses, the relative contribution of blood flow and O₂ extraction to the regulation of tissue O₂ delivery being determined by the prevailing venous oxygen level. The previous study (2) has shown that in skeletal muscle perfused with constant pressure, both reactive hyperemia and elevated arteriovenous (A-V) O₂ difference contribute to the O₂ debt repayment following arterial occlusion when the initial A-V O₂ difference is in the normal range. However, at low prevailing A-V O₂ difference, increased O₂ extraction is the major mechanism by which the tissue repays its O₂ debt and the contribution of blood flow is minimal. As the prevailing venous O₂ reserve is lowered, the contribution of O₂ extraction diminishes and reactive hyperemia becomes more important for the compensation. Thus, the immediate post-occlusion O₂ extraction is only slightly elevated or even transiently depressed.