小鼠脑梗死模型神经源性心脏损害机制探讨

MECHANISM OF NEUROGENIC HEART DAMAGE IN A MOUSE MODEL OF CEREBRAL INFARCTION

目的探讨小鼠脑梗死神经源性心脏损害机制。方法建立小鼠脑梗死模型（n=30）,分别于脑梗死后24、72、120 h处死小鼠,每次10只,处死前,使用预冷注射器从小鼠颈动脉采血1 mL。处死后,立即取出心脏,储存于-70℃液氮中。测定其血浆和心脏组织中肾上腺素、去甲肾上腺素及血浆磷酸激酶同工酶（CK-MB）水平,以假手术组小鼠30只作为对照。结果脑梗死组24、721、20 h血浆和心肌组织肾上腺素、去甲肾上腺素以及血浆CK-MB水平均高于假手术组,差异有显著性（t=2.32-2.64,P〈0.05）。脑梗死组血浆及心肌组织肾上腺素、去甲肾上腺素水平72 h最高,24 h次之,120 h最低,差异有显著意义（F=3.02-3.72,q=3.02-6.42,P〈0.05）。脑梗死组24、721、20 h血浆CK-MB水平比较,差异无显著性（P〉0.05）。假手术组血浆和心肌组织各检测指标24、72、120 h比较差异无显著性（P〉0.05）。结论血浆和心肌组织中肾上腺素、去甲肾上腺素水平升高可能是导致小鼠缺血性脑卒中神经源性心脏损害的原因。

Objective To explore the mechanism of neurogenic heart damage in a mouse model of cerebral infarction（CI）. Methods A mouse model of CI was created in 30 mice,which were sacrificed at 24,72 and 120 hours,10 mice respectively,after infarction.Before sacrifice,1 mL of blood was taken from carotid artery,and the heart removed,stored in-70 ℃ liquid nitrogen,immediately as the mouse was killed.The epinephrine and norepinephrine levels in plasma and heart tissue were measured with HPLC method,and plasma CK-MB levels detected with immunosuppression method.Thirty mice in sham-operation group were served as the control. Results The epinephrine and norepinephrine levels in plasma and heart tissue,and plasma CK-MB of the 24-,72-,and 120-hour group were significantly higher than that in the control（t=2.32-2.64,P〈0.05）.In the CI group,the epinephrine and norepinephrine levels in plasma and heart tissue were the highest at 72 hours,the next was at 24 hours,and that of the lowest at 120 hours,the differences between them being significant（F=3.02-3.72,q=3.02-6.42,P〈0.05）.In sham-operation,various items,detected at 24,72 and 120 hours,showed no significant differences（P〉0.05）. ConclusionThe increase of epinephrine and norepinephrine levels in plasma and heart tissue might be the cause resulting in neurogenic heart damage in mice following cerebral arterial thrombosis.