ABSTRACT
This chapter argues that supports the view that the hyperdynamic circulation of chronic portal hypertension plays a major role in increased intravascular pressure. Emphasis is also placed on intestinal transvascular exchange and mechanisms responsible for the alterations in gastrointestinal blood flow that accompany acute and chronic portal hypertension. The reduced precapillary resistance is responsible for the higher capillary pressure in chronic portal hypertension when compared to an equivalent degree of acute portal hypertension. Another possible explanation for the intestinal vasodilation of chronic portal hypertension is the release of vasodilator metabolites from the tissue since acute portal hypertension is known to increase oxygen consumption in the small intestine of both dogs and cats. Therefore, it seems unlikely that the response of the intestinal vasculature to chronic portal hypertension could be explained in terms of a metabolic mechanism. Moment to moment control of splanchnic blood flow is accomplished through integration of intrinsic and extrinsic control systems.
