Effects of norepinephrine on oxygenation of resting skeletal muscle

Abstract

Effects of arterial infusions of norepinephrine (NE) were studied in the canine skinned hindlimb. Myoglobin PO2 [O2 partial pressure] changes were estimated from shifts of CO between blood and muscle. At an NE concentration just below threshold for an effect on vascular resistance, myoglobin PO2 and O2 uptake rate (.ovrhdot.VO2) did not change. At NE concentrations at which vascular resistance increased 117-216% and blood flow (.ovrhdot.Q) fell to 55-88% of control, O2 extraction per unit flow increased but myoglobin PO2 and .ovrhdot.VO2 did not change significantly. At higher NE concentrations, with vascular resistance 197-1178% and blood flow 17-55% of control, CO shifted out of blood into tissue, indicating a fall in myoglobin PO2, and O2 uptake rate fell as a function of .ovrhdot.Q, despite increases in O2 extraction per unit flow. During these high-concentration NE infusions, the tissue became hypoxic under conditions in which femoral venous PO2 was much greater than is seen during arterial hypoxemia experiments. NE at concentrations at which there were modest effects on vascular resistance probably did not interfere with normal autoregulation of intracellular PO2, suggesting that constriction of resistance vessels did not alter the capillary recruitment mechanism. The inability of skeletal muscle to maintain intracellular PO2 during high NE concentrations under conditions in which maximal extraction of O2 was not achieved is best explained by an effect of NE on the capillary recruitment mechanism.