Pérez López Silvia, Otero Hernández Jesús, Vázquez Moreno Natalia, Escudero Augusto Dolores, Alvarez Menéndez Francisco, Astudillo González Aurora
Unidad de Coordinación de Trasplantes y Terapia Celular, Hospital Universitario Central de Asturias, Oviedo, Spain.
J Heart Lung Transplant. 2009 Aug;28(8):815-20. doi: 10.1016/j.healun.2009.04.021.
Brain death (BD) causes hemodynamic and neuroendocrine alterations including a catecholamine surge, which in turn causes histologic lesions in cardiac muscle such as contraction bands, focal mononuclear cell infiltrates and cardiomyocyte necrosis. These changes are likely to compromise heart function and could therefore also affect the graft response after heart transplantation. This study was designed to examine the catecholamine surge, the catecholamine release pattern and the histologic lesions traditionally described as characteristic of BD in hearts procured from BD donors.
After BD diagnosis, specimens were taken from the left ventricle (n = 50) for histologic examination. Arterial blood samples were collected from 40 of the donors at different time-points (1 hour before BD; on BD diagnosis; and 1, 2, 3 and 4 hours after BD) to determine catecholamine levels by high-performance liquid chromatography (HPLC).
The three hormones examined showed above-normal levels (epinephrine 2.36-fold, norepinephrine 8.56-fold, dopamine 54.76-fold). Release patterns included epinephrine and dopamine peaks at the time of BD and a norepinephrine peak 1 hour later. Fifty percent of the BD donors showed contraction bands and 62% displayed cardiomyocyte necrosis, which was associated with focal mononuclear cell infiltrates in 18% of cases. In 40% of donors, colocalized apoptotic and necrotic damage was observed.
Differing extents of BD-associated cardiac lesions were observed in the donors, and >50% also showed apoptotic damage. The expected catecholamine peak at the time of BD was only detected for epinephrine and dopamine. Hormone increases were below those described in the literature, except for dopamine.
脑死亡（BD）会引起血流动力学和神经内分泌改变，包括儿茶酚胺激增，进而导致心肌出现组织学病变，如收缩带、局灶性单核细胞浸润和心肌细胞坏死。这些变化可能会损害心脏功能，因此也可能影响心脏移植后的移植物反应。本研究旨在检测从脑死亡供体获取的心脏中儿茶酚胺激增情况、儿茶酚胺释放模式以及传统上被描述为脑死亡特征的组织学病变。
在诊断脑死亡后，从左心室采集标本（n = 50）进行组织学检查。在不同时间点（脑死亡前1小时；脑死亡诊断时；脑死亡后1、2、3和4小时）从40名供体采集动脉血样本，通过高效液相色谱法（HPLC）测定儿茶酚胺水平。
所检测的三种激素水平均高于正常（肾上腺素升高2.36倍，去甲肾上腺素升高8.56倍，多巴胺升高54.76倍）。释放模式包括脑死亡时肾上腺素和多巴胺出现峰值，去甲肾上腺素在1小时后出现峰值。50%的脑死亡供体出现收缩带，62%表现出心肌细胞坏死，其中18%的病例伴有局灶性单核细胞浸润。在40%的供体中，观察到凋亡和坏死损伤共存。
在供体中观察到不同程度的与脑死亡相关的心脏病变，超过50%的供体还表现出凋亡损伤。仅在肾上腺素和多巴胺中检测到脑死亡时预期的儿茶酚胺峰值。除多巴胺外，激素升高幅度低于文献报道。
