Woods W T, Chapman G D
Magnesium. 1985;4(2-3):96-101.
This study was designed to test the hypothesis that Mg++ prevents the electrophysiologic changes caused by hypoxia in cardiac cells. Canine right ventricular false tendons (32 hearts) were pinned to the floor of a tissue bath and suffused with physiologic solution. Microelectrodes recorded the spontaneous action potentials. The isolated tissue was exposed to a hypoxic solution (PO2 less than 50 mm Hg) containing either normal [Mg++] (0.85 mmol/l) or high [Mg++] (3.4 mmol/l). Hypoxia with normal [Mg++] caused increased firing rate (+40%), depolarization of the resting (maximum diastolic) potential (from-72 to -55 mV), and reduction in amplitude (from 88 to 76 mV). The depolarization, reduction in amplitude, and most of the increased firing rate were completely blocked when [Mg++] was elevated to 3.4 mmol/l; propranolol (10 mg/l) blocked the residual increase in firing rate.
本研究旨在验证镁离子可防止心肌细胞缺氧所致电生理变化这一假说。将犬右心室假腱索（32个心脏）固定于组织浴槽底部，并用生理溶液灌注。微电极记录自发动作电位。将分离的组织暴露于含正常镁离子浓度（0.85 mmol/L）或高镁离子浓度（3.4 mmol/L）的缺氧溶液（氧分压小于50 mmHg）中。正常镁离子浓度下的缺氧导致发放率增加（+40%）、静息（最大舒张期）电位去极化（从-72 mV至-55 mV）以及幅度降低（从88 mV至76 mV）。当镁离子浓度升至3.4 mmol/L时，去极化、幅度降低以及大部分发放率增加均被完全阻断；普萘洛尔（10 mg/L）可阻断发放率的残余增加。
