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冠状动脉内注射镁对局部缺血再灌注犬心脏的急性再灌注损伤并无保护作用。

Intracoronary magnesium is not protective against acute reperfusion injury in the regional ischaemic-reperfused dog heart.

作者信息

Schlack W, Bier F, Schäfer M, Uebing A, Schäfer S, Borchard U, Thämer V

机构信息

Abt. für Herz- und Kreislaufphysiologie, Heinrich-Heine-Universität, Dusseldorf, Germany.

出版信息

Eur J Clin Invest. 1995 Jul;25(7):501-9. doi: 10.1111/j.1365-2362.1995.tb01736.x.

Abstract

Intravenous magnesium lowers mortality in patients with suspected myocardial infarction. We tested the hypothesis that the protective effect may be due to a direct, local influence of magnesium on myocardial reperfusion injury in a dog model of ischaemia/reperfusion. Ten anaesthetized open chest dogs underwent 1 h of left anterior descending artery (LAD) occlusion and 6 h of reperfusion. The animals received intracoronary (i.c.) magnesium aspartate (Mg, n = 5) or vehicle infusion (n = 5) for the first hour of reperfusion. Mg infusion was adapted to actual LAD flow (ultrasonic flow probe) to increase regional plasma concentration by 4 mmol L-1. Regional myocardial function was measured as percent systolic wall thickening (sWTh, sonomicrometry). Intracoronary Mg increased LAD flow during application (at 15 min reperfusion; Mg, 194 +/- 44 (mean +/- SD); control, 116 +/- 41 mL min-1 100 g-1, P < 0.01). sWTh decreased during coronary occlusion from 14.3 +/- 7.1% to -4.7 +/- 2.7% in the control group and from 14.8 +/- 2.5% to -4.1 +/- 3.1% in the Mg group. Throughout the reperfusion period wall function remained depressed in both groups to a similar degree (control, -3.5 +/- 1.8%; Mg, -3.0 +/- 1.9% at 6 h reperfusion). Global haemodynamics were not different. Infarct size after 6 h reperfusion (TTC staining) was similar in both groups (Mg, 20.6 +/- 5.0; control, 24.4 +/- 8.7% of area at risk). Regional magnesium application (i.c.) to post-ischaemic reperfused myocardium had no influence on infarct size or post-ischaemic regional wall function in this model.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

静脉注射镁可降低疑似心肌梗死患者的死亡率。我们在缺血/再灌注犬模型中检验了以下假设:这种保护作用可能是由于镁对心肌再灌注损伤的直接局部影响。十只麻醉开胸犬接受左前降支动脉(LAD)闭塞1小时和再灌注6小时。在再灌注的第一小时,动物接受冠状动脉内(i.c.)注入天冬氨酸镁(Mg,n = 5)或注入赋形剂(n = 5)。镁注入量根据实际LAD血流量(超声血流探头)进行调整,以使局部血浆浓度增加4 mmol/L。局部心肌功能通过收缩期壁增厚百分比(sWTh,超声心动图)来测量。冠状动脉内注入镁在注入期间增加了LAD血流量(再灌注15分钟时;Mg组,194±44(平均值±标准差);对照组,116±41 mL·min⁻¹·100 g⁻¹,P < 0.01)。在冠状动脉闭塞期间,对照组的sWTh从14.3±7.1%降至 -4.7±2.7%,镁组从14.8±2.5%降至 -4.1±3.1%。在整个再灌注期,两组的壁功能均以相似程度持续降低(再灌注6小时时,对照组为 -3.5±1.8%;镁组为 -3.0±1.9%)。整体血流动力学无差异。再灌注6小时后的梗死面积(TTC染色)在两组中相似(镁组为20.6±5.0;对照组为危险区域面积的24.4±8.7%)。在此模型中,对缺血后再灌注心肌进行局部镁应用(冠状动脉内)对梗死面积或缺血后局部壁功能无影响。(摘要截短于250字)

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