Cardiac dysfunction following brain death

脑死亡是一种中枢神经系统失去调节的情况。我们研究了中枢神经系统和脑死亡对心脏功能的影响1)心脏功能的中枢调节通过刺激中枢咪唑啉1受体激活迷走神经促进乙酰胆碱(Ach)的释放。ACh激活百日咳毒素敏感的G蛋白和蛋白激酶C，开放ATP敏感的K通道，激活心肌M受体，对氟烷-肾上腺素心律失常产生抗心律失常作用。此外，其机制还需要内源性一氧化氮(NO)，因为特异性的NO合成抑制剂(L-NAME、L-NMMA)取消了抗心律失常的作用。这些结果表明，脑死亡时迷走神经的心脏保护作用消失。2)脑死亡时挥发性麻醉剂的心肌敏化作用用改良的Pra…方法诱导脑死亡更多的tschke等人。(移植67：343-8,1999)。我们测定了脑死亡大鼠在0.3MAC氟烷、异氟烷和七氟醚存在时肾上腺素的致心律失常剂量，并将这些值与不使用麻醉剂时的值进行了比较。与未使用麻醉剂的大鼠相比，氟烷降低了肾上腺素的致心律失常剂量，而七氟醚和异氟醚也降低了肾上腺素的致心律失常剂量，但差异不显著。此外，脑死亡大鼠氟烷与异氟醚、氟烷与七氟烷致心律失常剂量的差异均小于幼鼠。这些结果提示，中枢神经系统可能参与了挥发性麻醉药的心肌敏化。3)脑死亡后的心功能我们用电导导管技术对大鼠的心功能进行了连续测定。直到脑死亡后约6小时，动脉血压才开始下降。然而，射血分数确实在脑死亡后2或3小时内减少。这些结果表明，心功能不全发生的时间远远早于血压显著下降的时间。三磷酸腺苷敏感性钾通道开放剂尼可地尔可延长脑死亡后射血分数降低的时间间隔，提高脑死亡后的存活率。三磷酸腺苷敏感性钾通道可能在脑死亡后心功能不全中起作用。较少

The brain death is a condition where regulation by the central nervous system was lost. We investigated effect of the central nervous system as well as the brain death on cardiac function.1) The central regulation of cardiac functionThe activation of the vagal nerve by stimulation of the central imidazoline 1 receptors facilitates acetylcholine (Ach) release. Ach stimulates myocardial muscarinic receptors following activation of pertussis toxin sensitive G protein, protein kinase C and opening ATP-sensitive K channels and produces antiarrhythmic action on halothane-epinephrine arrhythmias in rats. In addition, the mechanism requires endogenous nitric oxide (NO), because specific NO synthesis inhibitors (L-NAME, L-NMMA) abolished the antiarrhythmic effect. These results suggest that the cardiac protective effect by the vagal nerve abolished in the brain death condition.2) Myocardial sensitization of volatile anesthetics in brain deathBrain death was induced by the modified method of Pra … More tschke et al. (Transplantation 67:343-8, 1999) in rats. We examined the arrhythmogenic dose of epinephrine in the presence of 0.3 MAC of halothane, isoflurane and sevoflurane and compared these values with that in the absence of anesthetics in brain death rats. Halothane reduced arrhythmogenic dose of epinephrine compared with rats with no anesthetics, while sevoflurane and isoflurane also reduced the arrhythmogenic dose of epinephrine compared with rats with no anesthetics, but the difference was not significant. In addition, the differences of arrhythmogenic dose between halothane and isoflurane and between halothane and sevoflurane in the brain death rats were smaller than those in naive rats. These results suggest that the central nervous system may play a part in the myocardial sensitization of volatile anesthetics.3) Cardiac function following brain deathWe performed continuous measurement of cardiac function using conductance catheter technique in rats. Arterial blood pressure did not reduce until about 6 hours following brain death. However, ejection fraction did reduce 2 or 3 hours following brain death. These results suggested that cardiac dysfunction occurred much earlier than the significant blood pressure reduction. Nicorandil, an ATP sensitive K channel opener, prolonged the time interval to reduction of ejection fraction and improve the survival following brain death. ATP sensitive K channel may play a role in cardiac dysfunction following brain death. Less