Microvascular-extravascular mechanical coupling may protect the simply obstructed small intestine from mural strangulation

It is a common clinical notion that within the distended segment of small intestine proximal to a simple mechanical obstruction, elevated intraluminal pressure will compromise mural vascular perfusion and jeopardize mural viability. To investigate this assumption, we developed an experimental model of simple mechanical small bowel obstruction. In our experimental model, a segment of rat ileum approximately 3 cm. in length was isolated in-vivo. A single artery and single vein served as the only inlet and outlet to the mural microvascular bed; oneholed plugs tied into both ends of the segment provided access to a closed intraluminai volume. Total mural blood flow (Q) was measured by an ultrasonic flow probe on the small feeder artery, and total muraf vascular resistance (vascR) was calculated by dividing the pressure drop across the intestinal segment by the total mural blood flow. Q and vascR were recorded continuously as a function of time while we mimicked the distention of simple obstruction by adding boluses of volume intraluminally. Initially, following a distention step, Q decreased and vascR increased; however, Q and vascR significantly recovered toward their control values as the ileal segment relaxed. Such recovery refutes the notion that intestinal distention necessarily jeopardizes mural viability. We hypothesize that distention may effect changes in mural perfusion by means of the mechanical coupling between intramural microvessels and extravascular structures. We are currently investigating this coupling mechanism by infusing papaverine (a blocker of smooth muscle tone in both intramural microvessels and intestinal muscularis) into the mural circulation while we conduct our experimental trials. In the presence of papaverine, Q and vascR recovery can be explained only by the contribution of the mechanical coupling mechanism. Supported by NIH grant R37-HL-19039.