Vasodilator effects of desflurane and isoflurane in the feline small intestine.

The influence of desflurane (DES) and isoflurane (ISO) on the intestinal vasculature was investigated in normoventilated cats (n = 10) during basal chloralose anesthesia (control). We measured heart rate, mean arterial pressure (MAP), and intestinal blood flow (optical drop flowmetry). Intestinal vascular resistance (IVR) was derived. To avoid changes in local vascular tone related to alterations in transmural pressure gradients, intestinal arterial pressure was controlled and kept constant by a variable aortic clamp. Measurements were performed during control and during the administration of DES (3.5% and 7.0% end-tidal) or ISO (0.8% and 1.6% end-tidal). Each animal was exposed to both agents, prior to and after intestinal postganglionic denervation. In the innervated intestine, both DES and ISO dose-dependently decreased IVR. At the high dose, DES (50 +/- 10% decrease in IVR) was a significantly more powerful vasodilator than ISO (37 +/- 12% decrease in IVR). In the denervated intestine, less pronounced vasodilations were produced by both DES and ISO, as compared to the innervated state, and there were, in this situation, no significant differences between agents concerning the magnitude of the vasodilation. As indicated by comparisons between the innervated versus the denervated state, both neurogenic and non-neurogenic mechanisms contributed to the vasodilator responses. The vascular relaxation at the high dose was for ISO associated with a significantly more powerful non-neurogenic vasodilation, and for DES associated with a significantly more powerful neurogenic vasodilation. This suggests that withdrawal of sympathetic neurogenic vasoconstrictor tone is more important for the vasodilation produced by DES than it is for ISO.