摘要
目的 探讨异氟醚预处理对大鼠全脑缺血再灌注损伤的作用。方法 采用四动脉阻断法制作全脑缺血模型。选择雄性Wistar大鼠78只(250～300g)。随机分为四组:假手术组(SH,n=15)、缺血再灌注组(ISC,n=21)、缺血预处理组(IPC,n=21)、异氟醚预处理组(ISOPC,n=21)。每组按缺血后再灌注时间分为三个亚组:6h、24h、72h。脑组织标本切片后行HE染色观察海马CA1存活细胞数目、原位末端标记(TUNEL)法测定凋亡细胞。结果 HE染色:ISC组随再灌注时间延长CA1区存活的细胞数(个)由90±2(6h)减少至46±5(72h),P<0.01。与ISC组比较,IPC组和ISOPC组72h后CA1区大部分细胞存活,分别为82±4和80±5,P<0.01。TUNEL:ISC组再灌注6h后在CA1区起始段即开始有凋亡细胞,且数量随时间增加。而IPC组和ISOPC组在再灌注24h后出现少量凋亡细胞,再灌注72h后凋亡细胞百分数显著低于ISC组(P<0.01)。结论 异氟醚预处理通过抑制缺血诱导的神经细胞凋亡而产生保护作用。
Objective To investigate if isoflurane pretreatment can protect brain from bilateral hemispheric ischemia-reperfusion injury. Methods Seventy-eight male Wistar rats weighing 250-300 g were randomly divided into 4 groups : (A) sham operation group ( n = 15 ); (B) ischemia-reperfusion group (I/R, n = 21); (C) ischemia-preconditioning group (IP, n = 21) and (D) isoflurane pretreatment group (ISO, n = 21) Group B, C and D were further divided into 3 subgroups according to the duration of reperfusion 6 h, 24 h, 72 h. Global cerebral ischemia was produced by 4-artery occlusion technique. In sham operation group (A) bilateral vertebral and common carotid arteries were exposed but not occluded. In ischemia-reperfusion group (I/R) bilateral vertebral arteries were occluded by cauterization and bilateral common carotid arteries were exposed and clamped for 20 min, then undamped for reperfusion of different duration (6 h, 24 h and 72 h) . In ischemia-preconditioning group (C) ischemia-reperfusion was preceded by 3 min global ischemia. In isoflurane-pretreatment group (D) the animals inhaled 1,5% isoflurane for 2 h before I/R. The animals were sacrificed right after reperfusion and brain was removed immediately for microscopic examination of hippocampal CA1. The number of living neurons (HE staining) and apoptotic neurons (TUNEL) was counted. Results (1) In group B (I/R) the number of living neurons in CA1 was decreasing with duration of reperfusion from 90.2 ± 2.4 (after 6 h reperfusion) to 45.8 ?±4.9 (72 h of reperfusion) ( P < 0.01) ; while in group C (ischemia preconditioning) and D (isoflurane-pretreatment) the number of living neurons in CA1 after 72 h reperfusion was 82.1 ±4.1 and 79.9 ± 5.4 respectively. (2) In group B (I/R) the number of apoptotic neurons in CA1 increased with duration of reperfusion. The percentage of apoptotic neurons after 72 h of reperfusion was significantly lower in group C and D than that in group B. Conclusion Isoflurane pretreatment can protect brain by suppressing ischemia-induced neuronal apoptosis.
出处
《中华麻醉学杂志》
CAS
CSCD
北大核心
2003年第7期515-518,共4页
Chinese Journal of Anesthesiology
