Prielipp R C, Butterworth J F, Roberts P R, Black K W, Zaloga G P
Department of Anesthesia, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC 27157-1009, USA.
Anesth Analg. 1995 Jun;80(6):1083-7. doi: 10.1097/00000539-199506000-00003.
Patients with cardiac arrhythmias, ischemia, and infarction may benefit from administration of supplemental magnesium. However, the exact mechanisms for magnesium's beneficial effects remain unknown. Lysophosphatidyl choline (LPC), an amphipathic phospholipid released from cardiac cell membranes during ischemia, increases free intracellular calcium concentrations ([Ca]i) and has been implicated as a cause of cardiac arrhythmias and coronary artery spasm during myocardial ischemia. We postulated that magnesium acts by inhibiting cellular calcium overload induced by mediators such as LPC. Myocardial cells from male Sprague-Dawley rats were isolated from ventricular tissue samples and [Ca]i determined using the fluorescent dye, fura-2/acetoxymethyl ester, measured in a spectrofluorometer. The increase in [Ca]i after exposure to 100 and 200 microM LPC was recorded in cells suspended in modified Dulbecco's phosphate buffered saline solution with 0.2, 2.0, and 20 mM magnesium chloride. Differences were determined by analysis of variance with P < 0.05 considered significant. LPC significantly increased [Ca]i in the 100 microM (506 +/- 76 nM) and 200 microM (675 +/- 81 nM) concentrations, compared to baseline (301 +/- 25 nM). MgCl2 at both the 2.0 and 20 mM concentrations significantly blunted the increase in [Ca]i in myocardial cells exposed to LPC, whereas 0.2 mM MgCl2 was ineffective. LPC is a potent lipid mediator which increases myocyte [Ca]i in a concentration-dependent manner. Magnesium concentrations > or = 2.0 mM effectively antagonize the increase in [Ca]i induced by LPC. Thus, magnesium may limit intracellular calcium overload stimulated by ischemic-induced LPC release.
患有心律失常、缺血和梗死的患者可能会从补充镁中获益。然而，镁产生有益作用的确切机制仍不清楚。溶血磷脂酰胆碱（LPC）是一种在缺血期间从心肌细胞膜释放的两亲性磷脂，它会增加细胞内游离钙浓度（[Ca]i），并被认为是心肌缺血期间心律失常和冠状动脉痉挛的一个原因。我们推测镁通过抑制由LPC等介质诱导的细胞钙超载发挥作用。从雄性Sprague-Dawley大鼠的心室组织样本中分离出心肌细胞，使用荧光染料fura-2/乙酰氧基甲酯测定[Ca]i，并在荧光分光光度计中进行测量。将悬浮于含有0.2、2.0和20 mM氯化镁的改良杜氏磷酸盐缓冲盐溶液中的细胞暴露于100和200 μM LPC后，记录[Ca]i的增加情况。通过方差分析确定差异，P < 0.05被认为具有显著性。与基线（301 ± 25 nM）相比，100 μM（506 ± 76 nM）和200 μM（675 ± 81 nM）浓度的LPC显著增加了[Ca]i。2.0和20 mM浓度的MgCl2均显著减弱了暴露于LPC的心肌细胞中[Ca]i的增加，而0.2 mM MgCl2则无效。LPC是一种强效脂质介质，它以浓度依赖的方式增加心肌细胞[Ca]i。镁浓度≥2.0 mM可有效拮抗LPC诱导的[Ca]i增加。因此，镁可能会限制缺血诱导的LPC释放所刺激的细胞内钙超载。
