Mesenteric vasomotor effects of vasoactive intestinal polypeptide study on perfused isolated canine jejunal loops

The vasomotor effect of VIP on the mesenteric vascular bed was studied on isolated canine jejunal loops ex-vivo perfused at normothermia, under pulsatile flow with heparinized, oxygenated and non-recirculating whole blood. VIP has been administered intra-arterially either by 1 min injections or by long term infusions. The results showed that VIP dilates the mesenteric vascular bed. This effect appeared dose dependent up to concentrations of about 5 μg/ml of blood, value for which a maximal vasodepressor effect of 15 mm Hg±6 (S. D.) was reached. Long term infusions of VIP showed an “Escape” phenomenon: the arterial pressure — under constant flow — returned towards the resting level despite continued stimulation. During the vasodilating period induced by the polypeptide, the O2 consumption was increased. Such a response is not necessarily a result of a direct stimulation of specific metabolic processes, but might be related to an extension of the vascular bed by opening capillaries. Concerning the mode of action of the polypeptide, neither propanolol nor atropine were able to suppress the vasodepressor effect of VIP. A neuronal pathway therefore does not seem to be involved. Although, VIP acts directly on the mesenteric vascular bed, the present experimental procedures give no evidence for a significant physiological role of VIP in local regulation of mesenteric haemodynamics. This view is supported by the occurrence of an “Escape” phenomenon as well as by the high arterial concentrations needed for obtaining a significant vasodepressor effect.