AJP - Heart and Circulatory Physiology, Vol 253, Issue 5 1199-H1207, Copyright © 1987 by American Physiological Society
Does inadequate oxygen delivery trigger pressor response to muscle hypoperfusion during exercise?
D. D. Sheriff, C. R. Wyss, L. B. Rowell and A. M. Scher
Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle 98195.
In dogs running on a treadmill at 2 or 4 mph or 4 mph plus 10% incline,
graded reductions in hindlimb perfusion reflexly elicited pressor
responses. To test the idea that systemic arterial pressure (SAP) is raised
by accumulation in muscle of a nerve-activating "pressor substance" release
when O2 delivery becomes inadequate, arterial O2 content (CaO2) was reduced
29.1% by carbon monoxide (CO) inhalation before repeating exercise at 2
mph. We reasoned that the pressor substance, or related substances, should
appear in femoral venous blood and be correlated to SAP. [K+] behaved
inappropriately as a signal to raise SAP, i.e., when flow was reduced, SAP
rose markedly with little or no change in [K+]. SAP was well correlated to
pH and [lactate] over the three work loads. Compared with the same work
load with normal CaO2, CO shifted the relation between SAP and terminal
aortic flow rightward 0.30 l/min (34.5%) and the relation between SAP and
PO2 leftward 7.7 mmHg. CO did not affect the relation of SAP to terminal
aortic O2 delivery, hindlimb O2 uptake index, pH, or [lactate]. Thus
pressor responses are apparently generated when O2 delivery falls below
some critical level causing accumulation of a pressor substance the release
of which is linked to a metabolic event that precipitates lactate
accumulation.
