Atar D, Serebruany V, Poulton J, Godard J, Schneider A, Herzog W R
Department of Medicine, University of Maryland Medical Center, Baltimore 21201.
J Cardiovasc Pharmacol. 1994 Oct;24(4):603-11. doi: 10.1097/00005344-199410000-00011.
We tested the hypothesis that acute, intravenous (i.v.) magnesium (Mg2+) supplementation would protect against myocardial stunning in an in situ swine model of regional ischemia and reperfusion and that a concomitant inhibitory effect on platelet aggregation would be elicited. An open-chest model was used, with transient occlusion of the left anterior descending coronary artery (LAD) for 8 min. Regional contractile function was assessed by measuring wall thickening fraction with epicardial Doppler crystals. One control group (n = 6) and two treatment groups were studied: group I (n = 6) received 750 mg MgSO4 before occlusion; group II (n = 6) received 1 g MgSO4 after the occlusion. Both protocols produced significant hypermagnesemia. In group I, platelet aggregation was measured before and after Mg2+ treatment using platelet-rich plasma (PRP) and various agonists (ADP 5 and 10 mM and collagen 1 mg/ml). As compared with controls, both treatment groups experienced significantly less postischemic dysfunction, with systolic function returning more quickly to baseline. Furthermore, platelet aggregation was significantly decreased immediately after Mg2+ infusion. Inhibition of platelet aggregation induced by Mg2+ treatment occurs concomitantly with significant amelioration of postischemic myocardial dysfunction.
在局部缺血再灌注的原位猪模型中,急性静脉补充镁离子(Mg2+)可预防心肌顿抑,并且会引发对血小板聚集的抑制作用。采用开胸模型,使左冠状动脉前降支(LAD)短暂闭塞8分钟。通过用心外膜多普勒晶体测量室壁增厚分数来评估局部收缩功能。研究了一个对照组(n = 6)和两个治疗组:I组(n = 6)在闭塞前接受750 mg硫酸镁;II组(n = 6)在闭塞后接受1 g硫酸镁。两种方案均导致明显的高镁血症。在I组中,使用富含血小板血浆(PRP)和各种激动剂(5 mM和10 mM ADP以及1 mg/ml胶原蛋白)在镁离子治疗前后测量血小板聚集。与对照组相比,两个治疗组缺血后功能障碍均明显减轻,收缩功能更快恢复至基线。此外,镁离子输注后血小板聚集立即显著降低。镁离子治疗诱导的血小板聚集抑制与缺血后心肌功能障碍的显著改善同时发生。