Simas Rafael, Ferreira Sueli G, Menegat Laura, Zanoni Fernando L, Correia Cristiano J, Silva Isaac A, Sannomiya Paulina, Moreira Luiz F P
Laboratory of Cardiovascular Surgery and Circulation Pathophysiology (LIM-11), Instituto do Coração (InCor) do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, Brazil.
Clinics (Sao Paulo). 2015 Jun;70(6):446-52. doi: 10.6061/clinics/2015(06)11. Epub 2015 Jun 1.
Brain death is typically followed by autonomic changes that lead to hemodynamic instability, which is likely associated with microcirculatory dysfunction and inflammation. We evaluated the role of the microcirculation in the hemodynamic and inflammatory events that occur after brain death and the effects of autonomic storm inhibition via thoracic epidural blockade on mesenteric microcirculatory changes and inflammatory responses.
Male Wistar rats were anesthetized and mechanically ventilated. Brain death was induced via intracranial balloon inflation. Bupivacaine (brain death-thoracic epidural blockade group) or saline (brain death group) infusion via an epidural catheter was initiated immediately before brain death induction. Sham-operated animals were used as controls (SH group). The mesenteric microcirculation was analyzed via intravital microscopy, and the expression of adhesion molecules was evaluated via immunohistochemistry 180 min after brain death induction.
A significant difference in mean arterial pressure behavior was observed between the brain death-thoracic epidural blockade group and the other groups, indicating that the former group experienced autonomic storm inhibition. However, the proportion of perfused small vessels in the brain death-thoracic epidural blockade group was similar to or lower than that in the brain death and SH groups, respectively. The expression of intercellular adhesion molecule 1 was similar between the brain death-thoracic epidural blockade and brain death groups but was significantly lower in the SH group than in the other two groups. The number of migrating leukocytes in the perivascular tissue followed the same trend for all groups.
Although thoracic epidural blockade effectively inhibited the autonomic storm, it did not affect mesenteric hypoperfusion or inflammation induced by brain death.
脑死亡后通常会伴随自主神经变化，进而导致血流动力学不稳定，这可能与微循环功能障碍和炎症反应有关。我们评估了微循环在脑死亡后发生的血流动力学和炎症事件中的作用，以及通过胸段硬膜外阻滞抑制自主神经风暴对肠系膜微循环变化和炎症反应的影响。
雄性Wistar大鼠麻醉后进行机械通气。通过颅内球囊充气诱导脑死亡。在诱导脑死亡前立即经硬膜外导管注入布比卡因（脑死亡-胸段硬膜外阻滞组）或生理盐水（脑死亡组）。假手术动物作为对照组（SH组）。通过活体显微镜分析肠系膜微循环，并在诱导脑死亡180分钟后通过免疫组织化学评估黏附分子的表达。
脑死亡-胸段硬膜外阻滞组与其他组之间观察到平均动脉压行为存在显著差异，表明前一组经历了自主神经风暴抑制。然而，脑死亡-胸段硬膜外阻滞组中灌注小血管的比例分别与脑死亡组和SH组相似或更低。细胞间黏附分子1的表达在脑死亡-胸段硬膜外阻滞组和脑死亡组之间相似，但在SH组中显著低于其他两组。血管周围组织中迁移白细胞的数量在所有组中呈现相同趋势。
尽管胸段硬膜外阻滞有效地抑制了自主神经风暴，但它并未影响脑死亡诱导的肠系膜灌注不足或炎症反应。
