Intestinal blood flow autoregulation during foodstuff absorption

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Abstract
A version of the metabolic theory of autoregulation proposes that tissue oxygenation, not blood flow per se, is the controlled variable. If O2 delivery to tissue can be maintained by modulating O2 extraction, blood flow may change passively with manipulations of perfusion pressure. When O2 extraction is high, as in hypermetabolic states, a greater degree of control must be exerted over blood flow if O2 uptake is to be maintained. To test this prediction, isolated loops of canine small bowel were vascularly perfused as arteriovenous O2 difference, blood flow and perfusion pressure were recorded. Pressure-flow curves (P-F) were determined at standardized pressures of 180, 150, 120, 90 and 60 mm Hg. In the control situation P-F autoregulation was weak or absent. Passive responses predominated, i.e., the proportional change in flow was greater than the change in pressure. When metabolic rate was stimulated by placing transportable solutes in the gut lumen, P-F autoregulation became apparent between 120 and 90 mm Hg. At the step from 120-90 mm Hg, flow-regulating mechanisms compensated for nearly 50% of the imposed pressure reduction. Effects of elevating venous pressure were studied. In controls myogenic vasoconstriction was absent, but, when metabolic rate was increased, myogenic vasoconstriction followed venous pressure elevations. Apparently metabolic and myogenic mechanisms participate in local control of intestinal blood flow.

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