Shibata M, Ueshima K, Harada M, Nakamura M, Hiramori K, Endo S, Sato N, Mukaida H, Suzuki T, Suzuki T, Inada K
Iwate Medical University, Morioka, Japan.
Angiology. 1999 Jul;50(7):573-82. doi: 10.1177/000331979905000707.
Magnesium (Mg) inhibits the influx of calcium in vascular smooth muscle cells. The purposes of this study were to test the hypothesis that an intravenous administration of magnesium might effect the complement response and to determine the effects of a magnesium pretreatment of patients with acute myocardial infarction (AMI) on the incidence of reperfusion injuries. Thirty-eight AMI patients were treated with coronary reperfusion therapy within 6 hours of onset. They were randomly divided into two groups: group pretreated with intravenous magnesium sulfate (0.27 mmol/kg) (magnesium group, n = 19), and nonpretreated controls (placebo group). The reperfusion injuries observed within 1 hour after the coronary reperfusion included arrhythmias, aggravated chest pain, and ST segment elevation in 12-lead electrocardiograms. Coronary recanalization was performed in 36 patients. The incidence of reperfusion arrhythmia was significantly lower in the magnesium group than in the placebo group (17% vs 78%, p<0.001). At the postreperfusion stage, there was a tendency for the degree of ST segment reelevation in the magnesium group lower than in the placebo group (2.5 +/- 2.3 mm vs 4.7 +/- 3.8 mm, p = 0.07). No marked difference was observed in the incidence of chest pain aggravation between the two groups (67% vs 73%, ns). The peak serum levels of interleukin-6 (IL-6) were significantly lower in the magnesium group than those in the placebo group (38.9 +/- 25.0 vs 92.3 +/- 76.5 pg/mL, p = 0.016). The peak serum levels of matrix metalloproteinase-1 (MMP-1) were lower than those in the placebo group (16.2 +/- 4.8 vs 19.7 +/- 9.0 ng/mL, p = 0.09), but the difference was not significant. A positive correlation was observed between the peak MMP-1 values and the peak IL-6 values (r = 0.57, p = 0.001) in all patients. Increased serum ionized Mg2+ may inhibit arrhythmic recurrence and the production of IL-6 and MMP-1 after reperfusion and prevent the increase of myocardial lesions caused by calcium overload on myocytes. The increased IL-6 production may induce MMP-1, leading to tissue organ injury. Pretreatment with magnesium sulfate may protect the myocardium of AMI patients from reperfusion injuries.
镁（Mg）可抑制血管平滑肌细胞内钙的流入。本研究的目的是检验静脉注射镁可能影响补体反应这一假设，并确定急性心肌梗死（AMI）患者进行镁预处理对再灌注损伤发生率的影响。38例AMI患者在发病6小时内接受了冠状动脉再灌注治疗。他们被随机分为两组：静脉注射硫酸镁（0.27 mmol/kg）预处理组（镁组，n = 19）和未预处理的对照组（安慰剂组）。冠状动脉再灌注后1小时内观察到的再灌注损伤包括心律失常、胸痛加重以及12导联心电图ST段抬高。36例患者进行了冠状动脉再通。镁组再灌注心律失常的发生率显著低于安慰剂组（17%对78%，p<0.001）。在再灌注后期，镁组ST段再次抬高的程度有低于安慰剂组的趋势（2.5±2.3 mm对4.7±3.8 mm，p = 0.07）。两组间胸痛加重的发生率无明显差异（67%对73%，无统计学意义）。镁组血清白细胞介素-6（IL-6）的峰值水平显著低于安慰剂组（38.9±25.0对92.3±76.5 pg/mL，p = 0.016）。基质金属蛋白酶-1（MMP-1）的血清峰值水平低于安慰剂组（16.2±4.8对19.7±9.0 ng/mL，p = 0.09），但差异不显著。在所有患者中，MMP-1峰值与IL-6峰值之间存在正相关（r = 0.57，p = 0.001）。血清离子化Mg2+升高可能抑制再灌注后心律失常的复发以及IL-6和MMP-1的产生，并防止钙超载对心肌细胞造成的心肌损伤增加。IL-6产生增加可能诱导MMP-1，导致组织器官损伤。硫酸镁预处理可能保护AMI患者的心肌免受再灌注损伤。
