大蒜素在猪急性心肌梗死的导管模型中减弱再灌注无再流。

Yang Peng, Li Jiahui, Li Aili, Wang Yong, Shi Zaixiang, Ke Yuannan, Li Xianlun
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引用次数: 2

摘要

目的:探讨大蒜素对猪急性心肌梗死(AMI)模型再灌注无再流的减弱作用。方法:选取22头猪,假手术组6头,对照组和大蒜素组各8头。后两组用扩张球囊闭塞左冠状动脉前降支远端2小时,再灌注3小时。大蒜素组在再灌注前注射大蒜素(1.88mg/kg)至再灌注1小时。AMI前、闭塞后2小时、再灌注后3小时检查血流动力学数据。心肌超声造影(MCE)及病理染色评价心肌无回流区(NRA)。用放射免疫法检测血清促炎因子和内皮素-1。结果:再灌注后大蒜素组左室收缩压(LVSP)和左室舒张末期压(LVEDP)较对照组及AMI后2hr均有显著改善(p)。结论:大蒜素可能通过降低血清促炎因子和ET-1降低AMI猪导管模型的再灌注无再流。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Garlicin attenuates reperfusion no-reflow in a catheter-based porcine model of acute myocardial infarction.

Objective: To evaluate whether garlicin can attenuate reperfusion no-reflow in a catheter-based porcine model of acute myocardial infarction (AMI).

Methods: Twenty-two swine were used: six in a sham-operation group, and eight each in the control and garlicin groups. The distal part of the left anterior descending coronary artery (LAD) in the latter two groups was occluded by a dilated balloon for 2 hr, then reperfused for 3 hr. Garlicin (1.88mg/kg) was injected just before reperfusion until reperfusion for 1 hr in the garlicin group. Hemodynamic data were examined before AMI, 2 hr after occlusion, and 3 hr after reperfusion. Myocardial contrast echocardiography (MCE) and pathological staining were performed to evaluate the myocardial no-reflow area (NRA). Serum proinflammatory cytokines and endothelin (ET)-1 were examined by radioimmunoassay.

Results: Left ventricular systolic pressure (LVSP) and left ventricular end-diastolic pressure (LVEDP) significantly improved in the garlicin group after reperfusion compared with the control group and also 2hr after AMI (p<0.05 for both). MCE and pathological staining both showed garlicin attenuated reperfusion NRA after AMI (p<0.05, p<0.01). Garlicin not only decreased serum interleukin (IL)-6 and tumor necrosis factor (TNF)-α after reperfusion (p<0.05 for both), but also ET-1 level (p<0.01).

Conclusion: Garlicin attenuated reperfusion no-reflow in our catheter-based porcrine model of AMI, possibly through decreasing serum proinflammatory cytokines and ET-1.

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