Halothane 1.5 MAC, isoflurane 1.5 MAC, and the contractile responses of coronary arteries obtained from human hearts.

Active vasoconstriction of epicardial coronary arteries can cause myocardial ischemia in patients with coronary artery disease. Relief of vasoconstriction can improve blood flow to the heart. The purpose of this study was to determine if 1.5 MAC halothane and 1.5 MAC isoflurane would each attenuate contractions evoked by three putative mediators of coronary constriction in coronary arteries removed from the hearts of human beings. Hearts were obtained in the operating room from five patients undergoing cardiac transplantation and from six brain-dead patients undergoing organ donation procedures. Coronary arteries were dissected free, cut into rings, and studied in organ chambers. Endothelium-dependent relaxations to 10(-6) M bradykinin were examined; they indicated a variable degree of endothelial dysfunction in vessels used in the experiments. Contractile responses to 40 mM KCl were tested and were used as control contractions. Contractions evoked by serotonin, histamine, and prostaglandin F2 alpha were measured and were expressed as a percent of contractile responses evoked by 40 mM KCl. Halothane depressed the agonist-induced contractions. Maximal contractile responses to serotonin were 130% +/- 28% in untreated rings and 63% +/- 10% in rings exposed to halothane (P less than 0.03). Responses to histamine were 183% +/- 46% untreated and 121% +/- 26% during halothane administration (P less than 0.05), and responses to prostaglandin F2 alpha were 227% +/- 42% untreated and 148% +/- 18% with halothane (P less than 0.05). Isoflurane had no effect on contractions. The results demonstrate that 1.5 MAC halothane, but not 1.5 MAC isoflurane, attenuates contractile responses evoked by putative mediators of coronary vasoconstriction in coronary arteries removed from the hearts of human beings.