The control of the circulation in skeletal muscle during arterial hypoxia in the rabbit

Abstract

The effects of arterial hypoxia on muscle blood flow were examined in normal unanaesthetized rabbits in relation to simultaneously determined changes in cardiac output, arterial pressure and heart rate. Muscle blood flow was estimated from the difference between total limb flow (local thermodilution) and the estimated skin flow (using a calibrated heat conductivity method). The role of the arterial chemoreceptors and baroreceptors in the control of muscle blood flow was examined and the nature of the sympathetic efferent discharge analyzed. In mild hypoxia (O2 tension [PO2] > 35 mm Hg) in the rabbit, muscle blood flow did not change, although cardiac output increased. During moderate hypoxia (PO2 30 - 35 mm Hg) there was initial vasoconstriction in muscle, followed by a return to control values paralleling the changes in cardiac output. In severe arterial hypoxia (PO2 > 30 mm Hg) the initial vasoconstriction was less marked and during the steady state there was a large vasodilatation and increase in muscle blood flow, at a time when the cardiac output was not elevated. The early vasoconstriction in arterial hypoxia is mediated mainly through sympathetic vasoconstrictor nerves as a result of strong arterial chemoreceptor stimulation. Increased secretion of adrenaline is an important factor in restoring muscle blood flow to control values during moderate arterial hypoxia, and in elevating the muscle blood flow above these values in severe hypoxia. The peripheral dilator ([beta]-) effects of epinephrine oppose the peripheral constrictor ([alpha]-) effects resulting from increased activation of sympathetic constrictor nerves during arterial hypoxi.