Sevoflurane selectively increases coronary collateral blood flow independent of K-ATP channels in vivo

Background: Volatile anesthetic agents produce coronary vasodilation via ac tivation of adenosine triphosphate-sensitive potassium (K-ATP) channels. Th e authors tested the hypothesis that sevoflurane selectively increases coro nary collateral blood flow and assessed the role of K-ATP channel activatio n in this process. Methods: Experiments were conducted in dogs 8 weeks after long-term implant ation of a left anterior descending coronary artery (LAD) ameroid constrict or to stimulate coronary collateral growth, Dogs were instrumented for meas urement of retrograde LAD blood flow tan index of large coronary collateral blood flow) and LAD tissue flow (via radioactive microspheres; an index of small collateral blood flow). Coronary collateral perfusion and normal (le ft circumflex coronary artery [LCCA]) zone tissue blood flow were determine d in four groups of dogs pretreated with intracoronary glyburide (50 mu g/k g) or vehicle in the presence or absence of sevoflurane (1 minimum alveolar concentration). Dose-response relationships to the K-ATP channel agonist n icorandil were established in each dog using doses (25, 50, and 100 mu g/mi n) previously shown to increase coronary collateral blood flow. Results: Sevoflurane increased blood flow through large and small collatera ls and increased collateral vascular conductance in the presence of glyburi de but did not affect LCCA blood flow or conductance, In contrast, nicorand il increased blood flow through small but not large collaterals. Nicorandil also increased LCCA blood flow and conductance, actions that were attenuat ed by glyburide, Conclusions: The results demonstrate that sevoflurane selectively increases large and small coronary collateral blood flow via mechanism(s) independen t of K-ATP channel activation.