Roth A, Kornowski R, Agmon Y, Vardinon N, Sheps D, Graph E, Burke M, Laniado S, Yust I
Department of Cardiology, Tel-Aviv Elias Sourasky Medical Centre, Israel.
Eur Heart J. 1996 May;17(5):709-14. doi: 10.1093/oxfordjournals.eurheartj.a014937.
This study was designed to detect changes in complement levels following acute myocardial infarction and to test whether magnesium sulphate (MgSO4) administration interferes with the complement response that follows acute myocardial infarction.
Twenty-nine patients with acute myocardial infarction treated with streptokinase were included and randomly assigned to three treatment groups. In groups A and B, a bolus of 1 g MgSO4 was infused intravenously followed by 4 g (group A) and 14 g (group B) MgSO4 for 24 h while normal saline was administered in group C (control). Blood samples for C3, C4 and CH-100 were obtained at baseline and repeatedly during the 48 h following the initiation of magnesium infusion.
In groups A and C, a remarkable decrease in the levels of C3, C4 and CH-100 was observed when measured 1 h after the end of streptokinase infusion and thereafter for the ensuing 48 h compared to baseline values (P < 0.05). In group B, the decrease in these complement elements was attenuated, and a significant (P < 0.05) delayed decrease of C3 and C4 was observed only at 24 h and later up to 48 h. The mean level of CH-100 in group B was significantly depressed compared to baseline from 3 h and thereafter up to 48 h. Mean C3 values plotted against observation time differed between the three groups (P = 0.021). A similar trend was observed for C4 (P = 0.133) but not for CH-100 (P = 0.46).
(1) Complement elements are being consumed following acute myocardial infarction treated by streptokinase. (2) High-dose intravenous magnesium attenuates the complement process following acute myocardial infarction. (3) These results might signify that magnesium modulates the inflammatory response that follows infarction.
本研究旨在检测急性心肌梗死后补体水平的变化，并测试硫酸镁（MgSO4）给药是否会干扰急性心肌梗死后的补体反应。
纳入29例接受链激酶治疗的急性心肌梗死患者，并随机分为三个治疗组。A组和B组静脉注射1 g硫酸镁推注，随后A组给予4 g、B组给予14 g硫酸镁持续24小时，而C组（对照组）给予生理盐水。在基线时以及开始输注镁后的48小时内反复采集血液样本检测C3、C4和CH-100。
与基线值相比，A组和C组在链激酶输注结束后1小时及随后的48小时内，C3、C4和CH-100水平显著下降（P < 0.05）。B组中，这些补体成分的下降有所减轻，仅在24小时及之后至48小时观察到C3和C4显著（P < 0.05）延迟下降。B组CH-100的平均水平从3小时起至48小时与基线相比显著降低。三组之间绘制的平均C3值与观察时间不同（P = 0.021）。C4观察到类似趋势（P = 0.133），但CH-100未观察到（P = 0.46）。
（1）链激酶治疗的急性心肌梗死后补体成分被消耗。（2）大剂量静脉注射镁可减轻急性心肌梗死后的补体过程。（3）这些结果可能表明镁调节梗死后的炎症反应。
