THE ROLE OF OXYGEN IN ESCAPE OF SKELETAL MUSCLE ARTERIOLES FROM SYMPATHETIC NERVE STIMULATION (MICROCIRCULATION, BLOOD FLOW).

Abstract

In these experiments, we tested the hypothesis that sympathetic escape in skeletal muscle is mediated through a fall in parenchymal cell oxygen levels following blood flow reduction. This hypothesis predicts that if the fall in parenchymal cell PO₂ during stimulation can be minimized, escape should be reduced. To test this prediction, we studied the behavior of superficial arterioles of the cat sartorius muscle during 3 minutes of sympathetic nerve stimulation. The muscle was covered with silicone oil equilibrated with 0%, 5% and 10% oxygen. During stimulation under 0% oxygen, 90% of visible arterioles showed a significant secondary relaxation (escape). The relaxation averaged 55% of the initial constriction. Under 5% oxygen, resting arteriolar diameter was reduced by an average of 12% and escape was significantly reduced throughout the arteriolar network. Under 10% ambient oxygen, there was an additional 5% reduction in resting diameter and a further reduction of escape. Escape was not attenuated when control diameter was reduced to the same degree with arginine vasopressin, suggesting that the effect of oxygen was specific rather than secondary to an increase in vascular tone. The above observations are also consistent with the hypothesis that escape is mediated through a fall in vascular wall PO₂. To evaluate this possibility, periarteriolar and parenchymal tissue PO₂ were measured with oxygen microelectrodes during sympathetic stimulation under 0% and 10% oxygen suffusion of the muscle. In the proximal arterioles, the periarteriolar PO₂ during control and during stimulation was identical under 0% and 10% oxygen yet escape was reduced by 75% under 10% oxygen. Similarly, escape was reduced 90% in the distal arterioles under 10% oxygen but periarteriolar PO₂ was very nearly the same as that measured under 0% oxygen. In contrast, mean parenchymal tissue PO₂ fell to low levels during stimulation under 0% oxygen but did not fall below normal levels during stimulation under 10% oxygen. These findings argue against the hypothesis that a fall in vascular wall PO₂ is responsible for escape. The findings are consistent with the hypothesis that sympathetic escape in skeletal muscle is mediated through a fall in parenchymal cell PO₂. (Abstract shortened with permission of author.)