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芬太尼预处理对家兔急性失血性休克心肌损伤的影响 被引量:3

Effect of fentanyl pretreatment on myocardial injury induced by acute hemorrhagic shock in rabbits
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摘要 目的:观察芬太尼对急性失血性休克家兔心肌缺血缺氧性损伤的影响.方法:16只家兔随机分为生理盐水预处理组(C组)和芬太尼预处理组(F组).按照Wiggers改良法制作家兔失血性休克模型.放血前15min两组分别给予等容量的生理盐水和芬太尼,维持休克状态90min,记录放血前(T0),放血后15(T1),30(T2),45(T3),60(T4),75(T5)和90min(T6)时心功能指标的变化.于放血前(T0),放血后60min(T4)和90min(T6)时抽取动脉血用化学分光法测定血清心肌肌钙蛋白I(cTnI)的浓度,实验结束时取心尖部心肌组织行病理学电镜检查.结果:两组的血清cTnI的浓度在T2和T3时均比T1时显著增高(P<0.01),组间比较C组的血清cTn-I升高幅度明显高于F组(P<0.01);病理学电镜检查F组心肌损伤较C组减轻.结论:芬太尼预处理对家兔急性失血性休克后的心肌损伤有保护作用. AIM: To investigate the effect of fentanyl pretreat- merit on myocardial hypoxic-ischemic injury in rabbits with acute hemorrhagic shock. METHODS: Sixteen healthy white rabbits were randomly divided into 2 groups ( n = 8 ) : control group ( C group) and fentanyl pretreatment group (F group). Acute hemorrhagic animal models were established according to the Wigger's method. 15 min before bloodletting, the same volume of saline and fentanyl were given to group C and group F respectively. Keep the state of hemorrhagic shock for 90 min and take arterial blood before bloodletting ( T0 ) , 60 min after bloodletting ( T4 ) and 90 mln after bloodletting ( T6 ) for determination of serum cardiac Troponin I (cTnI) with chemiluminescence method. Heart functional parameters were recorded before bloodletting (T0 ) and 15 (T1), 30 (T2), 45 (T3), 60 (T4), 75 (T5) and90 (T6) min after bloodletting. Morphological change of the heart was observed by electron microscopy. RESULTS: The serum concentrations of cTnI increased significantly in the 2 groups at T2 and T3 as compared with T1 ( P 〈 0.01 ). cTnI values at T2 and T3 in group F were lower than those in group C ( P 〈 0.01 ). Myocardial injury in group F was less severe than that in group C. CONCLUSION: Fentanyl pretreatment can reduce myocardial injury induced by acute hemorrhagic shock in rabbits.
出处 《第四军医大学学报》 北大核心 2007年第1期79-81,共3页 Journal of the Fourth Military Medical University
关键词 芬太尼 失血性休克 心肌肌钙蛋白I 心肌损伤 fentanyl hemorrhagic shock cardiac troponin I myocardial injury
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