脑缺血再灌注大鼠脑SI区及视上核nNOS免疫阳性神经元的变化

目的：观察大鼠脑缺血再灌注后大脑皮质第一躯体感觉运动区（SI区）、视上核神经元型一氧化氮合酶（nitricoxidesynthase，nNOS）免疫阳性神经元形态、数量变化以探讨nNOS在缺血性脑损伤中的变化规律和作用。方法：健康SD大鼠84只，体重220—250g，随机分为2组：（1）脑缺血再灌注损伤模型组：用双侧颈总动脉阻塞法建立脑缺血再灌注损伤模型。（2）假手术组：只分离双侧颈总动脉而不阻断血流。分别于术后即刻、1、2、3d、1、2、4周灌注取脑，nNOS免疫细胞化学染色，观察大脑皮质SI区、视上核内nNOS免疫阳性神经元形态及数量变化。结果：结扎双侧颈总动脉后1、2d和2周，SI区nNOS免疫阳性神经元数量显著低于假手术组（P〈0．05）；结扎双侧颈总动脉后1周，视上核nNOS免疫阳性神经元数量显著低于假手术组（P〈0．05）。结论：脑缺血再灌注损伤后，SI区、视上核内nNOS免疫阳性神经元数量的减少可能参与了再灌注损伤的保护机制。

nNOS immunopositive neurons in sensorimotor cortex and supraoptic nucleus of rats with cerebral ischemia reperfusion injury

Objective： To study the morphology and number of nNOS immunopositive neurons in sensorimotor cortex （ S1 area） and supraoptie nucleus of rats with cerebral ischemia reperfusion injury, and to explore change and role of nNOS neurons in cerebral ischemia reperfusion injury. Methods：84 healthy SD rats, 220 g to 250g in weight, were randomized into two groups ： model group （ in which cerebral ischemia reperfusion injury were established by occlusion of bilateral common carotid arteries） and the sham operation group （in which bilateral common carotid arteries were dissected but not occluded）. The brain tissues of the rats were harvested for nNOS immunoeytochemical staining at several time points ： immediately after operation, days 1 through 3, weeks 1,2 and 4. The morphology and number of nNOS immunopositive neurons in $1 area and supraoptic nucleus in both groups were studied. Results：Significantly fewer nNOS immunopositive neurons in S1 area were observed in model rats than in sham-operated rats at ld, 2d and 2 weeks after ischemia reperfusion injury; fewer nNOS- positive neurons were also noted in supraoptic nucleus of rat models compared with as found for sham-operated rats at one week later after ischemia reperfusion injury （ P 〈 0.05 ）. Conclusion： The nNOS immunopositive neurons in S1 area and supraoptic nucleus decreased after cerebral isehemical reperfusion injury, which may be part of the protective mechanism against ischemia/reperfusion injury.