Codaccioni Jean-Laurent, Velly Lionel J, Moubarik Chahrazad, Bruder Nicolas J, Pisano Pascale S, Guillet Benjamin A
Laboratoire de Pharmacodynamie, UMR INSERM 608, Faculté de Pharmacie 27 bd, Jean Moulin, Marseille, France.
Anesthesiology. 2009 Jun;110(6):1271-8. doi: 10.1097/ALN.0b013e3181a1fe68.
Preconditioning the brain with volatile anesthetics seems to be a viable option for reducing ischemic cerebral injury. However, it is uncertain whether this preconditioning effect extends over a longer period of time. The purpose of this study was to determine if sevoflurane preconditioning offers durable neuroprotection against cerebral ischemia.
Rats (Sprague-Dawley) were randomly allocated to two groups: nonpreconditioned control group (n = 44) and preconditioned group (n = 45) exposed to 2.7 vol% sevoflurane (45 min) 60 min before surgery. Animals in both groups were anesthetized with 3.0 vol% sevoflurane and subjected to transient middle cerebral artery occlusion. After 60 min of awake focal ischemia, the filament was removed. Functional neurologic outcome (range 0-18; 0 = no deficit), cerebral infarct size (Nissl staining), and apoptosis (Terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate nick-end labeling; cleaved caspase-3 staining) were evaluated at 3, 7, and 14 days after ischemia.
Sevoflurane preconditioning significantly improved functional outcome and reduced infarct volume (109 +/- 43 vs. 148 +/- 56 mm(3)) 3 days after ischemia compared to the control group. However, after 7- and 14-day recovery periods, no significant differences were observed between groups. The number of apoptotic cells was significantly lower in the preconditioned group than in the control group after 3- and 7-day recovery periods. Fourteen days after ischemia, no differences were observed between groups.
In this model of transient focal cerebral ischemia, sevoflurane preconditioning induced effective but transient neuroprotective effects. Sevoflurane preconditioning also decreased ischemia-induced apoptosis in a more sustained way because it was observed up to 7 days after injury.
用挥发性麻醉剂对大脑进行预处理似乎是减少缺血性脑损伤的一种可行选择。然而，这种预处理效果是否能持续更长时间尚不确定。本研究的目的是确定七氟醚预处理是否能对脑缺血提供持久的神经保护作用。
将大鼠（Sprague-Dawley）随机分为两组：未预处理对照组（n = 44）和预处理组（n = 45），预处理组在手术前60分钟暴露于2.7体积%的七氟醚中（45分钟）。两组动物均用3.0体积%的七氟醚麻醉，并进行短暂性大脑中动脉闭塞。清醒状态下局灶性缺血60分钟后，取出栓线。在缺血后3天、7天和14天评估功能神经学结果（范围0 - 18；0 = 无缺陷）、脑梗死体积（尼氏染色）和细胞凋亡（末端脱氧核苷酸转移酶介导的缺口末端标记法；裂解的半胱天冬酶-3染色）。
与对照组相比，七氟醚预处理在缺血后3天显著改善了功能结果并减少了梗死体积（109±43 vs. 148±56 mm³）。然而，在7天和14天的恢复期后，两组之间未观察到显著差异。在3天和7天的恢复期后，预处理组的凋亡细胞数量明显低于对照组。缺血14天后，两组之间未观察到差异。
在这个短暂性局灶性脑缺血模型中，七氟醚预处理诱导了有效但短暂的神经保护作用。七氟醚预处理还以更持久的方式减少了缺血诱导的细胞凋亡，因为在损伤后7天仍可观察到这种作用。
