Observations on autoregulation in skeletal muscle: the effects of arterial hypoxia

Abstract

Autoregulation of blood flow in skeletal muscle, as manifested by steady-state resistance changes, has been shown to be present in the low range of perfusion pressure but has been demonstrated by some observers to be lacking at higher perfusion pressures. Transient responses have often been neglected or observed only qualitatively in analyses of autoregulation. The present study was undertaken (1) to determine the relative importance of steady-state and transient responses in flow in demonstrating autoregulation of blood flow over a broad range of perfusion pressures, (2) to establish a means of quantitating autoregulation, and (3) to observe the effect of hypoxia on autoregulation. In isolated, perfused canine gracilis muscle, perfusion pressure was increased and subsequently returned to baseline (9.7 ± 0.13 kPa [73 ±1 mmHg]) during perfusion with normally oxygenated blood (PO₂ = 9.3−13.3 kPa [70−100 mmHg]), and mildly (PO₂ = 6.1−9.2 kPa [46−69 mmHg]), moderately (PO₂ = 4.5−6.0 kPa [34−45 mmHg]), or severely (PO₂ = 2.7−4.4 kPa [20−33 mmHg]) hypoxic blood. Consistent with other studies canine gracilis muscle was often found to possess passive vascular responses when only steady-state parameters were considered. However, quantitation of the transient response in flow with step increases in perfusion pressure demonstrated substantial transient responses under conditions of normal oxygenation, and progressive attenuation of flow transients with increasing hypoxia.