大鼠脑缺血后心肌去甲肾上腺素的变化及再灌注对其的影响  

Changes of myocardial norepinephrine after cerebral ischemia and the effect of reperfusion on its expression

作　　者：王吉文[1] 蒋龙元[1] 丘宇茹[1] 陈玉成[1] 黄子通[1] 

机构地区：[1]中山大学附属第二医院急诊科,广州510120

出　　处：《中华神经医学杂志》2007年第12期1236-1239,1243,共5页Chinese Journal of Neuromedicine

摘　　要：目的探讨去甲肾上腺素(NE)在脑缺血期间心肌中的表达变化和再灌注对其的影响。方法将大鼠分成假手术组、缺血组、脑缺血再灌注组,分别测定脑缺血及脑缺血再灌注组0、6、12、24、48、72h的脑缺血面积、血清肌酸激酶同功酶(CK-MB)的浓度、心肌中NE的含量及心肌病理改变。结果脑缺血后6h可见缺血灶,12h达到峰值;血清中CK-MB浓度逐渐升高,12h达峰值,其后逐渐下降;心肌NE于6h达到峰值,12h开始下降。腩缺血再灌注后脑坏死面积显著减少(P<0.05);CK-MB浓度峰值时间不变,但6、12h均较脑缺血组显著增高(P<0.05);心肌NE峰值不变,但至48h仍持续高水平状态。心肌病理表现为炎性细胞浸润、心内膜炎、肌纤维变性、灶性坏死,偶见大而积心肌坏死;脑缺血再灌注后纤维变性和灶状坏死的总发生率明显增加。结论较大面积的脑缺血可使交感神经过度释放NE,导致继发心肌损伤;脑缺血再灌注可保护脑组织,但加重心肌中NE的释放,使心肌损伤加重。Objective To investigate changes of the expression of myocardial norepinephrine （NE） during cerebral ischemia and the effect of reperfusion on its expression. Methods Rats were randomly allocated into three groups： sham operation group, cerebral ischemia group and cerebral ischemia/reperfusion （I/R） group. The area of cerebral ischemia, concentration of serum CK-MB, content of myocardial NE and pathological changes of the myocardium were determined respectively for the cerebral ischemia group and I/R group （0, 6, 12, 24, 48 and 72 h）. Results The ischemic focus could be observed 6 h after cerebral ischemia and its area reached the peak value at 12 h; the concentration of serum CK-MB increased gradually after cerebral ischemia, peak at 12 h and later on, gradually declined; the content of myocardial NE peaked at 6 h and began to decline at 12 h. The cerebral necrotic area declined evidently after cerebral I/R; the peak time of the serum CK-MB concentration was unchanged, but concentrations after I/R were evidently higher than that in the cerebral ischemia group at 6 and 12 h; the peak time of myocardial NE was unchanged and the high level remained until 48 h. Pathological changes of the myocardium included inflammatory cell infiltration, endocarditis, myofibrosis and focal necrosis etc; large area of myocardial necrosis could be observed occasionally. The total incidence rate of myofibrosis and focal necrosis increased evidently after cerebral I/R. Conclusion Cerebral ischemia with comparatively larger area may induce excessive release of NE from sympathetic nerves, which could result in secondary myocardial injury. Cerebral I/R can protect brain tissues, but increases myocardial NE release, which thus aggravates myocardial injury.

关 键 词：缺血再灌注 心肌损伤 去甲肾上腺素 CK-MB 

分 类 号：R743.31[医药卫生—神经病学与精神病学]