Hypoperfusion of the intestinal microcirculation without decreased cardiac output during live Escherichia coli sepsis in rats.

In order to determine the intestinal microvascular responses to normotensive, high cardiac output (CO) bacteremia, we measured vascular diameters and blood flow at different levels of the intestinal microcirculation during live E. coli bacteremia in male Sprague-Dawley rats (n = 16). Precollicular brainstem transection was used to allow study free of drug anesthesia. The microcirculation of a loop of small intestine (with intact neurovascular connections) was observed by in vivo video microscopy and optical Doppler velocimetry at a magnification of x1,500. Intraluminal microvessel diameters and red cell velocity were measured in successive branches until the vessel entered a villus. CO was measured by transpulmonary thermodilution. Intravenous infusion of 1 x 10(9) live E. coli caused a 20% increase in CO at 50 min and a 14% decrease in systemic vascular resistance. However, microvascular blood flow to the small intestine decreased by 27% at 1 hr and by 56% at 2 hr. Progressive arteriolar constriction (25-50%, P less than .05) occurred at all levels of the intestinal microcirculation. These data indicate that intestinal hypoperfusion caused by arteriolar constriction occurs during high CO bacteremia. This hypoperfusion could contribute to mucosal injury and intestinal mucosal barrier dysfunction during sepsis.