Steady-state myogenic response of rat coronary microvessels is preserved by isoflurane but not by halothane.

The myogenic response of vascular smooth muscle produces vasomotion in response to changes in vessel transmural pressure. While this is an important determinant of coronary blood distribution, the effect of volatile anesthetics on the response has not been previously investigated. In this study, we examined the effect of isoflurane and halothane on this myogenic response. Coronary resistance arteries were isolated from Wistar rats. As the intraluminal pressure was increased from 10 to 120 mm Hg in the presence of either isoflurane (1%, 2%, and 3%), halothane (1% and 2%), or no volatile agent (control), the vessel intraluminal diameter was monitored using a video detection system. Passive changes in vessel diameter were measured after exposure to papaverine 100 microM. Additionally, the myogenic responses of endothelium-intact and endothelium-denuded vessels were compared. Endothelium-intact control vessels demonstrated myogenic constriction above 80 mm Hg of intraluminal pressure. This response was not affected by endothelial denudation. The response was preserved by isoflurane 1%, 2% or 3% but abolished by halothane 1% or 2%. We conclude that, in rat coronary resistance arteries, myogenic constriction can be demonstrated above 80 mm Hg of intraluminal pressure and is endothelium independent. This response is preserved by isoflurane but abolished by halothane. These findings may have implications for the effect of the anesthetics on coronary blood flow distribution.