Lockhart L K, Lautt W W
Department of Pharmacology and Therapeutics, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Am J Physiol. 1990 Oct;259(4 Pt 1):G605-10. doi: 10.1152/ajpgi.1990.259.4.G605.
The role of adenosine in hypoxia-induced vasodilation was examined in the intestine of pentobarbital sodium-anesthetized cats. A hollow-fiber fetal oxygenator was used to selectively reduce the PO2 of the blood supplying the superior mesenteric artery, thereby inducing hypoxia in the intestines. Decreasing the PO2 from 109 to 38 Torr caused vascular resistance to decrease from 10.2 to 7.5 Torr.kg.min.ml-1, a decrease of 2.7 Torr.kg.min.ml-1 or 24%. During selective adenosine receptor blockade with 8-phenyltheophylline, the same decrease in PO2 (from 109 to 40 Torr) produced a similar decrease in resistance from 5.7 to 3.4 Torr.kg.min.ml-1 or a difference of 2.3 Torr.kg.min.ml-1 (-36%). Thus adenosine is not the mediator of hypoxia-induced vasodilation in the feline intestine because blockade of the vasodilating effects of exogenous and presumably endogenous adenosine did not affect the observed decrease in resistance.