BACKGROUND: The coronary vascular endothelium could mediate some of the coronary effects of halogenated anaesthetic agents. The role of the endothelial vasodilator substances nitric oxide (NO) and prostaglandins (PGs) in the coronary effects of halothane and isoflurane remains to be determined and has not been investigated for desflurane. In this study, the roles of NO and cyclooxygenase pathways in the coronary effects of halothane, isoflurane and desflurane were studied in isolated red blood cell-perfused rabbit hearts. METHODS: Rabbit hearts were perfused by a Langendorf technique with red blood cells mixed with modified Krebs-Henseleit buffer. Coronary blood flow (CBF), oxygen consumption and myocardial performance were evaluated during exposure to 0.5, 1 and 2 rabbit minimum alveolar concentrations of halothane, desflurane and isoflurane. Thereafter, the same protocol was applied with the addition of N(G)-nitro-L-arginine (L-NNA), indomethacin or a combination of both inhibitors. RESULTS: Similar and significant increases in CBF were observed with increasing concentrations of isoflurane and desflurane. In contrast, CBF did not change with halothane. The combination of the two antagonists abolished desflurane-induced vasodilation, whereas it did not change the isoflurane-mediated increase in CBF. Halothane-induced vasoconstriction was observed in the presence of a combination of indomethacin with L-NNA. CONCLUSIONS: Halothane and desflurane induce the release of vasodilating prostaglandins and NO in rabbit coronary arteries. In contrast, these mediators are not involved in the coronary vasodilating properties of isoflurane.
BACKGROUND: The coronary vascular endothelium could mediate some of the coronary effects of halogenated anaesthetic agents. The role of the endothelial vasodilator substances nitric oxide (NO) and prostaglandins (PGs) in the coronary effects of halothane and isoflurane remains to be determined and has not been investigated for desflurane. In this study, the roles of NO and cyclooxygenase pathways in the coronary effects of halothane, isoflurane and desflurane were studied in isolated red blood cell-perfused rabbit hearts. METHODS:Rabbit hearts were perfused by a Langendorf technique with red blood cells mixed with modified Krebs-Henseleit buffer. Coronary blood flow (CBF), oxygen consumption and myocardial performance were evaluated during exposure to 0.5, 1 and 2 rabbit minimum alveolar concentrations of halothane, desflurane and isoflurane. Thereafter, the same protocol was applied with the addition of N(G)-nitro-L-arginine (L-NNA), indomethacin or a combination of both inhibitors. RESULTS: Similar and significant increases in CBF were observed with increasing concentrations of isoflurane and desflurane. In contrast, CBF did not change with halothane. The combination of the two antagonists abolished desflurane-induced vasodilation, whereas it did not change the isoflurane-mediated increase in CBF. Halothane-induced vasoconstriction was observed in the presence of a combination of indomethacin with L-NNA. CONCLUSIONS:Halothane and desflurane induce the release of vasodilating prostaglandins and NO in rabbit coronary arteries. In contrast, these mediators are not involved in the coronary vasodilating properties of isoflurane.