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

背景：脑死亡后大量儿茶酚胺释放被认为是心脏移植术后心功能障碍的重要原因之一。然而，脑死亡心脏发生心力衰竭的确切机制尚未完全阐明。本研究采用犬脑死亡模型，探讨冠状动脉对血管扩张剂的反应及其对血流动力学恶化的影响。方法：采用硬膜下球囊导管快速膨胀诱导脑死亡。对7只狗进行了血液动力学测量，包括利用压力-容量关系评估左心室收缩力和血液样本的生化分析。采用内皮依赖性（乙酰胆碱；乙酰胆碱）和非依赖性（硝普钠；SNP）冠状动脉血管舒张术评估8只狗的冠状动脉血流储备。结果：脑死亡诱导后出现短暂的高动力反应，随后动脉压、心输出量和冠状动脉血流量下降。脑死亡后60分钟左心室收缩力恶化。在脑死亡后30分钟和60分钟，乙酰胆碱和SNP的冠状动脉血流储备均显著受损（乙酰胆碱3μg至320.5%至189.1%和202.8%；SNP 100μg至255.6%至145.8%和153.5%）。冠状动脉阻力比在脑死亡后30分钟和60分钟显著增加。结论：脑死亡犬心脏冠状动脉血流储备及左心室功能受损。冠状动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.