Villeneuve E, Blaise G, Sill J C, Guerard M J, Buluran J, Girard D
Department of Anesthesiology, Université de Montréal, Quebec, Canada.
Anesth Analg. 1991 Apr;72(4):454-61. doi: 10.1213/00000539-199104000-00007.
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.
心外膜冠状动脉的主动血管收缩可导致冠心病患者发生心肌缺血。血管收缩的缓解可改善心脏的血流。本研究的目的是确定1.5最低肺泡有效浓度（MAC）的氟烷和1.5 MAC的异氟烷是否能减弱从人类心脏取出的冠状动脉中三种假定的冠状动脉收缩介质所诱发的收缩。心脏取自手术室中五名接受心脏移植的患者和六名接受器官捐献手术的脑死亡患者。将冠状动脉游离、切成环状，并在器官浴槽中进行研究。检测了对10(-6) M缓激肽的内皮依赖性舒张；结果表明实验中所用血管存在不同程度的内皮功能障碍。测试了对40 mM氯化钾的收缩反应，并将其用作对照收缩。测量了血清素、组胺和前列腺素F2α所诱发的收缩，并表示为40 mM氯化钾所诱发收缩反应的百分比。氟烷可抑制激动剂诱发的收缩。未处理环对血清素的最大收缩反应为130%±28%，而暴露于氟烷的环中为63%±10%（P<0.03）。对组胺的反应在未处理时为183%±46%，氟烷给药期间为121%±26%（P<0.05），对前列腺素F2α的反应在未处理时为227%±42%，氟烷处理时为148%±18%（P<0.05）。异氟烷对收缩无影响。结果表明，1.5 MAC的氟烷而非1.5 MAC的异氟烷可减弱从人类心脏取出的冠状动脉中假定的冠状动脉收缩介质所诱发的收缩反应。
