Affiliation:
1. Programs in Physiology and Pharmacology, The University of Texas Medical School at Houston and the Department of Biology, The University of Houston, Houston, Texas 77025
Abstract
Previous studies have shown that sympathetic stimulation can cause a redistribution of intestinal capillary blood flow. Our computer model of the intestinal circulation predicted that the diffusion parameters (e.g., capillary surface area and mean capillaryto-cell diffusion distance) altered by precapillary sphincter closure would be sufficient to affect intestinal oxygen extraction. To test this prediction in an animal model, we made continuous measurements of arteriovenous oxygen difference (ΔO
2
) and perfusion pressure during constant-flow perfusion of isolated loops of canine small bowel. Intraarterial infusion of norepinephrine or stimulation of sympathetic nerves for 7 minutes produced sustained increases in vascular resistance and sustained reductions in arteriovenous ΔO
2
. Maximal changes in resistance and arteriovenous ΔO
2
occurred by the second minute of norepinephrine or sympathetic nerve stimulation, and subsequently both parameters escaped somewhat. The maximal and steady-state values of these parameters were dose-dependent or frequency-dependent. In other experiments, sympathetic nerve stimulation caused synchronous decreases in arteriovenous ΔO
2
and
86
Rb extraction. These results support the hypothesis that the infusion of norepinephrine and the stimulation of sympathetic nerves cause sustained reductions in the density of the perfused capillary bed which are sufficient to reduce intestinal extraction of Rb and oxygen despite constant-flow perfusion.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Cardiology and Cardiovascular Medicine,Physiology
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