Effect of pulsatile pressure and metabolic rate on intestinal autoregulation

In the intestine, raising venous pressure elicits a precapillary vasoconstriction that has been ascribed to a myogenic mechanism. Such myogenic responses occur more frequently and have a greater magnitude if arterial pressure is pulsatile. This laboratory reported that the ability of the gut to autoregulate blood flow in response to perfusion pressure manipulations is enhanced if metabolic rate is stimulated by transportable intraluminal solutes. Since both myogenic and metabolic mechanisms may participate in local control, we attempted to delineate the relative contributions the two mechanisms make to autoregulation. In one set of experiments, pulse pressures of 20 and 40 mmHg evoked a slight but statistically significant vasoconstriction. In a second series of experiments, pressure-flow curves were determined in isolated canine small bowel. The ability of the gut to autoregulate was compared at pulse pressures of 0, 20, and 40 mmHg and at basal and elevated metabolic rates. Altering pulse pressure had no systematic effect on the ability of the intestine to autoregulate blood flow. In contrast, increasing metabolic rate consistently enhanced autoregulation at each of the pulse pressures studied. Therefore, these results indicate that although a myogenic mechanism may best account for the response to elevated venous pressure, autoregulation as expressed in pressure-flow curves is more strongly influenced by the prevailing metabolic rate than by stretch stimuli such as arterial pressure pulsations.