Intestinal capillary blood flow during metabolic hyperemia.

It has been postulated that local circulatory control mechanisms regulate the O2 flux to parenchymal cells by two vascular mechanisms: changes in blood flow that minimize capillary PO2 variations and changes in the density of the perfused capillary bed through which O2 extraction is regulated. To test this prediction, isolated loops of canine jejenum and ileum were perfused at either constant blood flow or constant pressure, and intraluminal glucose was used to increase metabolic rate. In the constant-flow series, glucose increased O2 extraction, O2 uptake, and rubidium extraction. Resistance fell when the metabolic rate was elevated. In the constant-pressure series, glucose increased blood flow, O2 extraction, O2 uptake, and capillary filtration coefficients. These results show that vascular resistance falls and that capillary density increases following an increase in oxygen demand. Thus, the glucose-stimulated gut loop seems to be a valid model of metabolic hyperemia, and its behavior would be difficult to reconcile with a purely myogenic theory of intestinal blood flow autoregulation.