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功能的影响。1)心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。乙酰胆碱刺激心肌毒蕈碱受体，激活百日咳毒素敏感的G蛋白、蛋白激酶C和打开atp敏感的K通道，对大鼠卤烷-肾上腺素心律失常产生抗心律失常作用。此外，其机制需要内源性一氧化氮（NO），因为特异性NO合成抑制剂（L-NAME, L-NMMA）可消除抗心律失常作用。这些结果表明迷走神经对心脏的保护作用在脑死亡状态下消失。2)挥发性麻醉药在脑死亡中的心肌致敏作用[j] . More tschke et al. （Transplantation, 67:343- 8,1999）。我们检测了0.3 MAC氟烷、异氟烷和七氟烷存在时脑死亡大鼠肾上腺素的致心律失常剂量，并将这些值与无麻醉剂情况下的值进行了比较。氟烷较未麻醉大鼠降低肾上腺素致心律失常剂量，七氟醚和异氟醚也较未麻醉大鼠降低肾上腺素致心律失常剂量，但差异不显著。此外，脑死亡大鼠的氟烷与异氟烷、氟烷与七氟烷致心律失常剂量差异小于幼稚大鼠。这些结果提示中枢神经系统可能在挥发性麻醉药的心肌致敏中起作用。3)脑死亡后的心功能我们用导尿管技术连续测量大鼠的心功能。动脉血压直到脑死亡后约6小时才降低。然而，在脑死亡后2或3小时，射血分数确实降低。这些结果表明，心功能障碍的发生要比血压显著降低早得多。尼可地尔是一种ATP敏感的K通道打开剂，可延长射血分数降低的时间间隔，提高脑死亡后的生存率。ATP敏感的K通道可能在脑死亡后心功能障碍中起作用。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