Thämer V, Grunert S, Bier F, Schlack W
Institut für Herz- und Kreislaufphysiologie, Heinrich-Heine-Universität, Düsseldorf.
Herz. 1997 Jun;22 Suppl 1:35-9. doi: 10.1007/BF03042653.
In addition to its antiarrhythmic and antithrombotic effects magnesium is said to have a beneficial effect in patients with acute myocardial infarction. Magnesium can protect myocardial tissue after coronary occlusion and reduces infarct size in experimental models of ischaemia and reperfusion, though the given doses of magnesium are relatively high and differ from clinically reachable serum concentrations. We tested 2 hypotheses in a dog model of ischaemia-reperfusion: 1. The protective effect may be due to a direct, local influence of magnesium on myocardial reperfusion injury. 2. Systemic magnesium treatment with low doses comparable to clinical study regiments may reduce myocardial infarct size. Anaesthetized open chest dogs underwent 1 h of left anterior descending artery occlusion followed by 6 h of reperfusion. 1. Ten animals received intracoronary magnesium aspartate (Mg i.c.) or vehicle infusion (control i.c.) for the first hour of reperfusion to increase regional Mg-concentration by 2 mmol/l. 2. Fourteen animals received intravenous infusion with magnesium potassium aspartate (Mg-K i.v.) or vehicle infusion (control i.v.), beginning 1 h before occlusion until the end of the 6 h reperfusion period. Regional magnesium concentration in the Mg i.c.-group increased to 2.7 +/- 1.00 mmol/l at 45 min of reperfusion. Intravenous infusion raised serum magnesium from 0.71 +/- 0.03 mmol/l to 1.29 +/- 0.14 mmol/l in the Mg-K i.v. group (5 min of reperfusion, p < 0.01 vs. baseline). Infarct size after 6 h reperfusion (TTC staining) was similar in both groups of intracoronary treatment (Mg i.c., 20.6 +/- 5.0; control, 24.4 +/- 8.7% of area at risk; p = n.s.) and intravenous treatment (Mg-K i.v. 18.1 +/- 14.8; control 14.1 +/- 12.2% of area at risk; p = n.s.). Neither regional nor systemic magnesium leads to a clinically relevant reduction of infarct size in the regional ischaemic-reperfused dog heart when it is given in clinically usable doses. The beneficial action of systemic Mg is probably not due to an early direct protective effect on ischaemic-reperfused myocardium but to its antiarrhythmic and antithrombotic effects. Possibly only to high doses of Mg applied under experimental conditions can reduce infarct size.
除了其抗心律失常和抗血栓形成作用外，镁据说对急性心肌梗死患者也有有益作用。在缺血和再灌注的实验模型中，镁可以在冠状动脉闭塞后保护心肌组织并减小梗死面积，尽管所给予的镁剂量相对较高，且与临床上可达到的血清浓度不同。我们在缺血-再灌注犬模型中测试了两个假设：1. 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。2. 与临床研究方案相当的低剂量全身镁治疗可能会减小心肌梗死面积。麻醉开胸犬接受1小时左前降支动脉闭塞，随后再灌注6小时。1. 十只动物在再灌注的第一小时接受冠状动脉内注入天冬氨酸镁（Mg i.c.）或赋形剂输注（对照i.c.），以使局部镁浓度增加2 mmol/l。2. 十四只动物在闭塞前1小时开始接受静脉输注天冬氨酸镁钾（Mg-K i.v.）或赋形剂输注（对照i.v.），直至6小时再灌注期结束。在再灌注45分钟时，Mg i.c.组的局部镁浓度增加到2.7±1.00 mmol/l。静脉输注使Mg-K i.v.组的血清镁从0.71±0.03 mmol/l升高到1.29±0.14 mmol/l（再灌注5分钟时，与基线相比p<0.01）。两组冠状动脉内治疗（Mg i.c.，20.6±5.0；对照，危险区域面积的24.4±8.7%；p=无统计学意义）和静脉治疗（Mg-K i.v. 18.1±14.8；对照14.1±12.2%危险区域面积；p=无统计学意义）在再灌注6小时后的梗死面积相似。当以临床可用剂量给予时，局部或全身镁均不会导致局部缺血-再灌注犬心脏的梗死面积出现临床上相关的减小。全身镁的有益作用可能不是由于对缺血-再灌注心肌的早期直接保护作用，而是由于其抗心律失常和抗血栓形成作用。可能只有在实验条件下应用的高剂量镁才能减小梗死面积。
