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

冠状动脉血流对脑死亡所致左心室收缩功能障碍的影响

• 批准号: 11671331
• 负责人: MORITA Shigeki
• 金额: $ 2.3万
• 依托单位: Kyushu University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1999
• 资助国家: 日本
• 起止时间: 1999 至 2000
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11671331/
• 关键词: Brain death; Coronary artery; Coronary flow reserve; Endothelium; Cardiac function; 血管内皮機能

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.

背景资料：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。本研究的目的是探讨冠状动脉血管扩张剂的反应和血流动力学恶化的贡献使用犬脑death model.Methods：脑死亡引起的硬膜下放置的球囊导管的快速膨胀。在7只犬中进行血液动力学测量，包括使用压力-容积关系评估左心室收缩力和血液样品的生化分析。冠状动脉血流储备评估内皮依赖性（乙酰胆碱;乙酰胆碱）和非依赖性（硝普钠; SNP）的冠状动脉vasodilationin 8只犬。结果：高动力反应，观察到短暂的诱导脑死亡后，动脉压，心输出量和冠状动脉血流量下降。脑死亡后60分钟左心室收缩力下降。脑死亡后30分钟和60分钟，Ach和SNP均使冠状动脉血流储备明显受损（Ach 3μg分别为320.5%和202.8%，SNP 100μg分别为255.6%和145.8%和153.5%）.结论：脑死亡犬心脏冠状动脉血流储备和左室功能均受损。这种受损的冠状动脉循环可能不利于心功能不全的保存和恢复。