O2 delivery and the venous PO2-O2 uptake relationship in pump-perfused canine muscle

Abstract

Under the conditions of both an increased red cell affinity for O2 at a constant rate of O2 delivery (arterial O2 content x flow) and a decrease in the rate of O2 delivery induced by hypoxic hypoxia at constant blood flow, we have obtained a linear relationship between the partial pressure of O2 in the muscle venous effluent (Pv,O2) and O2 uptake (VO2). The relationship is described by the equation VO2 = Da × Pv,O2 + VO2,conv where Da is the apparent O2 diffusion capacity and VO2,conv is O2 delivery-limited VO2, and Da × Pv,O2 represents the O2 diffusion-limited VO2 (VO2,diff). From these observations, we propose the hypothesis that VO2 consists of two additive values, VO2,conv and VO2,diff. The mechanism underlying the reduction in VO2 that is induced by reducing O2 delivery to markedly below the VO2,conv value has only been investigated using a model based on the single compartment of diffusion-limited VO2, and has not been investigated in terms of this additive VO2 model. The single compartment analysis appears to overestimate the role of O2 diffusion in limiting the reduction of VO2 that occurs in response to a decrease in O2 diffusion capacity, as reflected by the VO2/Pv,O2 ratio. To gain better insight into the mechanism involved, we altered the rate of O2 delivery by changing arterial PO2 from normoxia (with inhalation of air) to hypoxia (by inhalation of 10-11 % O2) and blood flow (with high and low flow rates (n = 7 for both groups), and very low and ischaemic flow rates (n = 4 for both groups)) in pump-perfused dog gastrocnemius preparations during tetanic isometric contractions at 1 Hz. As rates of O2 delivery were reduced from 23.2 to 10.9 ml min-1 (100 g)-1, significant decreases in Pv,O2 and VO2 were observed (P < 0.05). From the data of Pv,O2 and VO2 values within this range of O2 delivery rates, we obtained the regression equation VO2 = 0.22 × Pv,O2 + 8.14 (r = 0.58). From the equation, the intercept of the VO2-axis was significantly different from zero (P < 0.05), in accordance with the observation that the VO2/Pv,O2 ratio (ml min-1 (100 g)-1 Torr-1) increased from 0.54 to 1.35 (P < 0.05). However, at extremely low rates of O2 delivery (5.6 and 7.3 ml min-1 (100 g)-1 the VO2/Pv,O2 ratio was 1.51 and 2.80 (P < 0.05), respectively. This indicates a break in the linear VO2-Pv,O2 relationship as the rate of O2 delivery was reduced to below the VO2,conv value of the VO2-axis intercept. These results suggest that the reduction in VO2 caused by extreme reductions in the rate of O2 delivery is not attributable to a reduction in O2 diffusion capacity, as expected from the VO2/Pv,O2 ratio, but to a reduction in the O2 delivery-limited VO2 component, as evaluated by the VO2-axis intercept of the linear VO2-Pv,O2 relationship.