摘要
目的 研究异氟烷预适应对心内直视手术中缺血 /再灌注对心肌损伤的保护作用及可能机制。方法 择期行先天性心脏病矫正术的患者 4 0例 ,随机分为异氟烷预适应组 (I组 ,n =2 0 )和对照组 (C组 ,n =2 0 )。两组病人均采用相同剂量芬太尼麻醉(30 μg·kg-1) ,其中异氟烷预适应组在主动脉阻断前吸入 10min 1MAC的异氟烷 ,随后继以 5min的洗脱期 ,而对照组只给予15min的纯氧吸入。观察麻醉前 (T0 ) ,主动脉开放后即刻 (T1)、2h(T2 )、6h(T3 )、2 4h(T4)、4 8h(T5)、各时点的血浆肌酸激酶同工酶 (CK MB) ,心肌肌钙蛋白I(cTnI)水平以及主动脉开放后心脏自主复跳率。结果 预适应组在主动脉开放后血浆CK MB(T2 ,T3 )及cTn I(T1~T5)浓度与对照组相比有显著降低 (P <0 0 5 ) ,并且心脏自主复跳率有显著增高。结论 在临床心内直视手术中 ,由缺血 /再灌注造成的损伤 ,异氟烷预适应可以产生和缺血预适应相似的心肌保护作用。
Aim To evaluate the myocardial protection of isoflurane preconditioning against ischemia-reperfusion injury and investigate the probably mechanism of this effect.Methods Forty patients undergoing open heart surgery with cardiopulmonary by-pass(CPB)were divided randomly into two groups: isoflurane preconditioning group (group I) and control group (group C).The patients of both group D and group C were anesthetized with high dose fentanyl(30 μg·kg -1 ).The patients of group D underwent 10 min of 1 minimal alveolar concentration(MAC) of isoflurane followed by 5 min washout before aorta clamping,but the group C only underwent 15 min 100% O 2 before aorta clamping.The central venous blood samples were collected for the measurement of CK-MB and myocardiac troponin I(cTnI) level before anesthesia(T 0)and immediately(T 1),2 h(T 2),6 h (T 3),24 h(T 4),48 h(T 5) after aorta in opening.The rate of spontaneously rebeating of hearts were observed after aorta opening.Results After reperfusion,the concentration of CK-MB(T 2,T 3)and cTnI (T 1~T 5)n group I were significantly decreased than those in group C, meanwhile, the rate of spontaneously rebeating of hearts in group I was higher than that in group C. Conclusion These results indicate that pre-ischemic administration of isoflurane dose cause anaesthetic-induced preconditioning to protect myocardium against ischemia-reperfusion injury.
出处
《安徽医药》
CAS
2004年第6期411-412,共2页
Anhui Medical and Pharmaceutical Journal
关键词
异氟烷
麻醉药预适应
心肺转流术
缺血/再灌注损伤
肌钙蛋白Ⅰ
isoflurane
anesthetic preconditioning
cardiopulmonary by-pass
ischemia-reperfusion injury
myocardiac troponin I