氟烷和七氟醚对缺血心肌功能和代谢及Ca2+-ATP酶活性的影响

目的: 研究氟烷、七氟醚(1.5MAC)对缺血心肌的影响。方法: 应用离体大鼠心脏Langendorff逆行灌注模型研究氟烷、七氟醚对心肌缺血前心率(HR)、左室舒张末期压力(LVEDP)、左室发展压(LVDP)、左室压力升高速率(+dp/dt)、左室压力下降速率(-dp/dt)和冠脉流量(CF)的影响,测定缺血前、缺血10min、缺血25min3个不同时间的心肌ATP含量、Ca²⁺-ATP酶活性,同时记录缺血间期左室内压的变化情况。结果: 七氟醚显著增加正常离体心脏的CF,氟烷、七氟醚均不同程度地抑制心肌收缩功能和Ca²⁺-ATP酶活性,能够增加正常心肌的能量贮备。缺血10min时,二药能够减缓心肌ATP含量及Ca²⁺-ATP酶活性的下降,氟烷的作用比较明显。缺血间期,氟烷明显推迟缺血性挛缩的起始时间,降低挛缩幅度。结论: 氟烷的抗缺血损伤作用优于七氟醚,延缓缺血期心肌ATP含量及Ca²⁺-ATP酶活性的下降可能是氟烷抗缺血损伤作用的重要机制之一。

Effects of halothane and sevoflurane on the function, metabolism and Ca2+-ATPase activity of ischemic myocardium

AIM: To study the effects of 1.5 MAC halothane and sevoflurane on ischemic myocardium. METHODS: The isolated rat heart were perfused with halothane and sevoflurane and HR, LVEDP, LVDP, +d p /d t , -d p /d t , coronary flow (CF), the myocardial ATP content and Ca 2+ -ATPase activity were determined before and 10 min and 25 min after ischemia. In the meantime, LVP was recorded during 25 min ischemia. RESULTS: 1.5MAC sevoflurane significantly increased CF in normal isolated rat hearts. Both halothane and sevoflurane depressed myocardial contractile function, increased normal myocardial energy storage. After 10 min ischemia, the decrease of myocardial ATP content were slowed down by halothane and sevoflurane, especially halothane. During 25 min of ischemia, the onset time of contracture was significantly delayed, and the contracture intensity was alleviated by halothane, but not sevoflurane. CONCLUSION: Halothane has better protective effect on ischemic myocardium than sevoflurane through preventing the decrease of myocardial ATP content and Ca 2+ -ATPase activity during ischemia.