Effects of halothane, isoflurane and sevoflurane on calcium-related contraction in porcine coronary arteries

Background: Volatile anaesthetics have a direct inhibitory effect upon epicardial coronary arterial smooth muscles (1–4). The site and mode of their action at the cellular level need to be clarified, which was the purpose of our study. The present investigation attempted to answer the question in what way volatile anaesthetics influence Ca²⁺-related contraction in isolated porcine epicardial coronary to understand their intracellular mechanism. Methods: Isolated helical strips of porcine epicardial coronary artery without endothelium were suspended for isotonic contraction recordings in Krebs-Ringer's solution. 9.4×10^-2 MK+, 2.5×10^-1 M Ca²⁺-induced shortening of the strips was regarded as the reference value (100%). After incubation in Ca²⁺-free solution with 10^-3 M ethlene glycol bis (β-aminoethyl ether)-N, N-tetraacetic acid (EGTA) for 60 minutes, the muscle strips were exposed to increasing Ca²⁺ concentrations (10^-4-10^-2) either in the presence or absence of 1.5 or 2.5 minimum alveolar concentration (MAC) halothane, isoflurane or sevoflurane, with 9.4×10^-2 M K⁺ bath solution. Results: All three drug groups produced apparent biphasic effects with a cumulative increase of Ca²⁺ concentration compared with control groups. An initial increase at low Ca²⁺ concentration was followed by a decrease of Ca²⁺-activated contractions. Isoflurane affected Ca²⁺-induced contraction significantly more than halothane and sevoflurane. Conclusions: The results imply that volatile anaesthetics influence Ca²⁺-dependent activity of coronary smooth muscle by complex mechanisms, which involve promotion of intracellular Ca²⁺ release and other mechanisms that alter sensitivity to calcium.