Silva I A, Correia C J, Simas R, Cruz J W M C, Ferreira S G, Zanoni F L, Menegat L, Sannomiya P, Moreira L F P
Laboratory of Cardiovascular Surgery, Heart Institute (InCor) of Sao Paulo University Medical School, Sao Paulo, Brazil.
Transplant Proc. 2012 Sep;44(7):2213-8. doi: 10.1016/j.transproceed.2012.07.108.
After brain death (BD) donors usually experience cardiac dysfunction, which is responsible for a considerable number of unused organs. Causes of this cardiac dysfunction are not fully understood. Some authors argue that autonomic storm with severe hemodynamic instability leads to inflammatory activation and myocardial dysfunction.
To investigate the hypothesis that thoracic epidural anesthesia blocks autonomic storm and improves graft condition by reducing the inflammatory response.
Twenty-eight male Wistar rats (250-350 g) allocated to four groups received saline or bupivacaine via an epidural catheter at various times in relation to brain-death induction. Brain death was induced by a sudden increase in intracranial pressure by rapid inflation of a ballon catheter in the extradural space. Blood gases, electrolytes, and lactate analyses were performed at time zero, and 3 and 6 hours. Blood leukocytes were counted at 0 and 6 hours. After 6 hours of BD, we performed euthanasia to measure vascular adhesion molecule (VCAM)-1, intracellular adhesion molecule (ICAM)-1, interleukin (IL)-1β, tumor necrosis factor (TNF)-α, Bcl-2 and caspase-3 on cardiac tissue.
Thoracic epidural anesthesia was effective to block the autonomic storm with a significant difference in mean arterial pressure between the untreated (saline) and the bupivacaine group before BD (P < .05). However, no significant difference was observed for the expressions of VCAM-1, ICAM-1, TNF-α, IL-1β, Bcl-2, and caspase-3 (P > .05).
Autonomic storm did not seem to be responsible for the inflammatory changes associated with BD; thoracic epidural anesthesia did not modify the expression of inflammatory mediators although it effectively blocked the autonomic storm.
脑死亡（BD）供体通常会出现心脏功能障碍，这导致大量器官未被利用。这种心脏功能障碍的原因尚未完全明确。一些作者认为，伴有严重血流动力学不稳定的自主神经风暴会导致炎症激活和心肌功能障碍。
探讨胸段硬膜外麻醉通过减轻炎症反应来阻断自主神经风暴并改善移植物状况的假说。
28只雄性Wistar大鼠（体重250 - 350克）被分为四组，在与脑死亡诱导相关的不同时间通过硬膜外导管接受生理盐水或布比卡因。通过在硬膜外空间快速充气使球囊导管导致颅内压突然升高来诱导脑死亡。在0、3和6小时进行血气、电解质和乳酸分析。在0和6小时计数血液白细胞。脑死亡6小时后，实施安乐死以测量心脏组织上的血管细胞黏附分子（VCAM）-1、细胞间黏附分子（ICAM）-1、白细胞介素（IL）-1β、肿瘤坏死因子（TNF）-α、Bcl-2和半胱天冬酶-3。
胸段硬膜外麻醉有效地阻断了自主神经风暴，在脑死亡前未治疗组（生理盐水）和布比卡因组之间平均动脉压有显著差异（P <.05）。然而，在VCAM-1、ICAM-1、TNF-α、IL-1β、Bcl-2和半胱天冬酶-3的表达上未观察到显著差异（P >.05）。
自主神经风暴似乎与脑死亡相关的炎症变化无关；胸段硬膜外麻醉虽然有效地阻断了自主神经风暴，但并未改变炎症介质的表达。
