Effect of coronary artery flow on left ventricular contractile dysfunction induced by brain death

背景：脑死亡后大量的儿茶酚胺释放被认为是心脏移植后心功能不全的重要原因之一。然而，脑死亡心脏心力衰竭的确切机制尚未完全阐明。本研究的目的是利用犬脑死亡模型研究冠状动脉对血管扩张剂的反应及其在血流动力学恶化中的作用。对7只狗进行了血流动力学测量，包括利用压力-容量关系评价左心室收缩能力和血液样本的生化分析。用血管内皮依赖性(乙酰胆碱；Ach)和非内皮依赖性(硝普钠；SNP)扩张冠脉评价8只犬的冠脉血流储备。结果：脑死亡诱导后出现一过性高动力反应，动脉压、心输出量和冠脉血流量下降。脑死亡后60分钟，左心室收缩功能开始恶化。在脑死亡后30分钟和60分钟，Ach和SNP的冠脉血流储备均显著受损(Ach 3μg 320.5%至189.1%和202.8%；SNP 100μg 255.6%至145.8%和153.5%)。在脑死亡后30分钟和60分钟，冠脉阻力比显著增加。结论：脑死亡犬存在冠脉血流储备和左心功能受损。冠脉循环受损可能不利于心功能障碍的保存和恢复。

Background : Massive catecholamine release after brain death is thought to be one of the most important causes to cardiac dysfunction after heart transplantation. However, the exact mechanism for cardiac failure in brain-dead heart has not been fully elucidated. The aim of this study was to investigate the response of coronary artery to vasodilator and their contribution to hemodynamic deterioration using canine brain death model.Methods: Brain death was induced by rapid inflation of a subdurally placed balloon catheter. Hemodynamic measurements including assessment of left ventricular contractility using pressure-volume relations and biochemical analysis of blood samples was performed in 7 dogs. Coronary flow reserve was assessed by endothelium-dependent (acetylcholine ; Ach) and -independent (sodium nitroprusside ; SNP) coronary vasodilation in 8 dogs.Results: Hyperdynamic response was observed transiently after induction of brain death followed by decreases in arterial pressure, cardiac output and coronary blood flow. Left ventricular contractility was deteriorated at 60-minute after brain death. Coronary flow reserve both by Ach and SNP were significantly impaired at 30- and 60-minute after brain death (Ach 3μg 320.5 % to 189.1 % and 202.8 % ; SNP 100μg 255.6 % to 145.8 % and 153.5 %). Coronary resistance ratios were significantly increased at 30- and, 60-minute after brain death.Conclusions : Impairement of coronary flow reserve and left ventricular function was observed in brain-dead canine heart. This impaired coronary circulation could be a disadvantage of preservation and recovery of cardiac dysfunction.