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关键词： 心肺复苏(CPR) ,神经内分泌反应
心脏骤停(CA)及心肺复苏(CPR)过程中，机体经历完全血液停止、严重缺氧、酸中毒和缺血再灌注等一系列剧烈的应激过程。大量的神经内分泌因子参与了这一过程。这些因子间相互作用，对CA的病理生理改变，对复苏药物的应用效果和CPR的预后产生重要影响。
1 下丘脑-垂体-肾上腺轴的功能
在CA时及给予肾上腺素和恢复自主循环后1小时内，用放免的方法多次测量病人促肾上腺皮质激素(ACTH)及可的松血清浓度，结果在死亡组ACTH和可的松浓度显著低于成功复苏组［1］。更进一步将CA时和其它应激情况下病人的可的松浓度作比较，发现CA病人可的松浓度明显减低［2］。在CPR及恢复自主循环后作促皮质醇激发试验，73%的恢复自主循环病人起始可的松血清浓度＞20 ng，且在恢复自主循环后第6小时显著增加，53%的未成功复苏病人可的松浓度＜20 ng，在6小时和24小时可的松浓度＜30 ng者死亡率分别是96%和100%。提示虽然在CA时有巨大的肾上腺交感反应，但下丘脑-垂体-肾上腺轴的功能仍明显受损、低下，这一功能的受损所致的ACTH和可的松的浓度的减低，可影响重要生命器官的灌注，进而影响成功的复苏，其在恢复自主循环后的血液动力学不稳定性中有重要生命器官的灌注，进而影响成功的复苏，其在恢复自主循环后的血液动力学不稳定性中有重要的病理意义。下丘脑-垂体-肾上腺轴的功能受损过程和CPR的预后明显相关。
脑垂体对低灌注的另一个重要反应为精氨酸加压素(AVP)升高。这在出血动物模型及CA病人都已得到了证实［3］。在CPR时及在有自主循环的情况下，血浆AVP浓度与主动脉压呈正相关，而高主动脉压可使垂体得到良好的血液灌注，因而引起AVP的高循环水平。AVP的高水平或者是能够改善灌注压，或者是灌注压改善的结果。进一步的研究证实AVP增加拟肾上腺素药物的加压反应［4］，它还可增加外周血管阻力而减少心排血量。这可作为CA时理论上理想的升压药物。因为外周阻力的增高与恢复自主循环呈正相关，而且它的降低心脏正性肌力的作用也降低了心肌耗氧量，改善心肌的供氧和需氧平衡。AVP并不象肾上腺素类药物一样具有心率加快的作用，这使得它可能成为CPR时有效的升压药物。特别是AVP与肾上腺素并用时其效果已得到证实［4，21］。
目录：
1 下丘脑-垂体-肾上腺轴的功能
2 内源性血管加压素及其病理生理作用
3 前列腺素及血栓素对CPR的影响
4 心钠素(ANP)对CPR影响
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