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卡托普利在溶栓和再灌注过程中不影响血浆内皮素-1。

Captopril does not affect plasma endothelin-1 during thrombolysis and reperfusion.

作者信息

Di Pasquale P, Paterna S, Parrinello G, Bucca V, Cannizzaro S, Pipitone F, Maringhini G, Scalzo S, Licata G

机构信息

Division of Cardiology, G.F. Ingrassia Hospital, Palermo, Italy.

出版信息

Int J Cardiol. 1995 Sep;51(2):131-5. doi: 10.1016/0167-5273(95)02418-v.

DOI:10.1016/0167-5273(95)02418-v
PMID:8522408
Abstract

Studies showed that endothelin-1 (ET-1) was increased in the acute myocardial infarction (AMI). Experimental studies reported that captopril was able to reduce ET-1 secretion, and that ET-1 was increased during reperfusion. This study was aimed to verify if captopril was able to reduce plasma ET-1 during thrombolysis in AMI. Seventy-three patients, hospitalized for suspected AMI within 4 h from the onset of symptoms suitable for thrombolysis (1st episode), Killip class 1-2, were randomized (double blind) into two groups: group 1 (37 pts), 8 F/29 M, received captopril, 6.25 mg, orally 15 min before thrombolysis. Group 2: (36 pts) 8 F/28 M, received placebo before thrombolysis. All patients met the reperfusion criteria. Plasma ET-1 were checked on admission, at 1 h and at 2 h, after starting thrombolysis. Group 1 contained ten unstable angina, 17 anterior and ten inferior AMIs. Group 2 contained ten unstable angina, 16 anterior and ten inferior AMIs. Mean concentrations of ET-1: Unstable angina: group 1, basal--4.56, at 1 h--4.47, 2 h--5.89 pg/ml; group 2: basal--4.17, at 1 h--4.59, 2 h--5.24 pg/ml. Inferior AMI: group 1: basal--6.87, 1 h--7.75, 2 h--8.47; group 2: basal--6.34, 1 h--6.68, 2 h--7.98 pg/ml. Anterior AMI: group 1: basal--7.17, 1 h--7.93, 2 h--10.76 pg/ml (between basal and 2-h samples P < 0.05); group 2: basal--7.46, 1 h--7.51, 2 h--10.74 pg/ml. Differences between the two groups were not significant. Our data suggest that captopril does not affect plasma ET-1 during thrombolysis.

摘要

研究表明,急性心肌梗死(AMI)时内皮素-1(ET-1)水平升高。实验研究报告称,卡托普利能够减少ET-1的分泌,且再灌注期间ET-1水平会升高。本研究旨在验证卡托普利在AMI溶栓过程中是否能够降低血浆ET-1水平。73例因症状发作后4小时内疑似AMI住院且适合溶栓(首次发作)、Killip分级为1 - 2级的患者,被随机(双盲)分为两组:第1组(37例),8例女性/29例男性,在溶栓前15分钟口服6.25毫克卡托普利。第2组(36例),8例女性/28例男性,在溶栓前接受安慰剂。所有患者均符合再灌注标准。在入院时、开始溶栓后1小时和2小时检测血浆ET-1水平。第1组包括10例不稳定型心绞痛、17例前壁AMI和10例下壁AMI。第2组包括10例不稳定型心绞痛、16例前壁AMI和10例下壁AMI。ET-1的平均浓度:不稳定型心绞痛:第1组,基础值——4.56,1小时——4.47,2小时——5.89皮克/毫升;第2组:基础值——4.17,1小时——4.59,2小时——5.24皮克/毫升。下壁AMI:第1组:基础值——6.87,1小时——7.75,2小时——8.47;第2组:基础值——6.34,1小时——6.68,2小时——7.98皮克/毫升。前壁AMI:第1组:基础值——7.17,1小时——7.93,2小时——10.76皮克/毫升(基础值与2小时样本之间P < 0.05);第2组:基础值——7.46,1小时——7.51,2小时——10.74皮克/毫升。两组之间差异无统计学意义。我们的数据表明,卡托普利在溶栓过程中不影响血浆ET-1水平。

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