Experimental studies on the hemodynamics of the small intestine following increased intraluminal pressure

Experimentally, we produced obstruction of the intestine in dogs, and the intraluminal pressure of the small intestine was measured without inducing anesthesia and with the abdominal wall closed. The maximum active intraluminal pressure reached 44.1 +/- 3.3 milligrams of mercury three days after the obstruction was produced. The pressure rose further to 95 millimeters of mercury, or higher, after an intravenous injection of physostigmine or during vomiting. When the intraluminal pressure is artificially increased and the vascular structure is observed by the resin-casting method, impairment of the villous circulation of the mucosa is already seen when the pressure reaches 20 millimeters of mercury. When the pressure was further increased, the circulation impairment spread toward the outer layer of the intestine. Mesenteric blood flow, peripheral vascular resistance and submucosal blood flow did not show significantly lower values than did the control group, unless the intraluminal pressure was 100 millimeters of mercury, or higher, but the oxygen consumption of the intestinal tissues was significantly lower than that for the control group when the intraluminal pressure was 40 millimeters of mercury, or higher. The resin-casting method showed that, at this pressure, a finding believed to indicate an arteriovenous shunt was already present at the mucosal villous base. The aforementioned results indicate that selective mucosal ischemia may occur when the intraluminal pressure increases to a range that is clinically possible when obstruction of the intestine occurs.