Abstract
The microvessels responsible for the major decrease in intestinal vascular resistance during the presence of glucose were defined. The normal distribution of tissue PO2 [O2 partial pressure] in the various layers of the intestinal tissue was measured at rest and during glucose exposure to determine if part of the absorptive hyperemia mechanism is related to a decrease in tissue PO2. In the rat small intestine, exposure of the mucosa only to glucose concentrations of 25-500 mg/100 ml causes a 20-25% dilation of all submucosal vessels in series with the mucosal vessels and mucosal arterioles. Total intestinal blood flow increased to 200-210% of control at all glucose concentrations. The tissue and perivascular PO2 in the villus apex decreased from 14.8 .+-. 1.2 (SE) mm Hg at rest to 6-8 mm Hg during glucose exposure; the PO2 in the muscle and submucosal layers tended to slightly increase above a normal of 26.4 .+-. 1.6 mm Hg during glucose exposure. Apparently virtually all intestinal arterioles are equally involved in absorptive hyperemia. The dilation of mucosal vessels may be related to a decrease in tissue PO2, but submucosal vessels dilate even though PO2 is slightly increased.