Siemkowicz E
King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia.
Resuscitation. 1997 Aug;35(1):53-9. doi: 10.1016/s0300-9572(97)00028-2.
This study in rats investigated the effects of 0.5 mEq/1 kg body weight of magnesium sulfate solution upon hypoxic left cardiac ventricular pressure (Part 1), optimal timing for injection of magnesium sulfate solution for successful resuscitation (Part 2) and survival benefits of magnesium sulfate after 8 or 12 min of hypoxia (Part 3) in rats resuscitated by single bolus arterial reperfusion using 2 ml of arterial blood and 6-9 micrograms epinephrine. A total of 153 pentobarbital anesthetized rats were subjected to 8 or 12 min 0.75% O2:99.25% N2 hypoxia in order to induce cardiac arrest. In Part 1, 13 rats (six control and seven injected with magnesium sulfate solution) were subjected to 12 min hypoxia and cardiac left ventricular pressure (LVP) was measured. In Part 2, 47 rats were exposed to 12 min of hypoxia. Normal saline or magnesium sulfate solution was injected prior to hypoxia, at 2 or 4 min of hypoxia, to find the optimal timing of magnesium sulfate injection for successful resuscitation by arterial reperfusion. In Part 3, 90 rats were studied to determine 7-day survival. Two control groups were injected with saline during 8 min (29 rats) or 12 min (18 rats) of hypoxia and two groups received magnesium sulfate solution during 8 min (14 rats) and 12 min (29 rats) of hypoxia. Magnesium sulfate fully reversed the hypoxic increase of LVP and improved survival after 12 min of hypoxia from approximately 15 (control) to 100% if given during the first 2.5 min of hypoxia. The main cause of the progressive resuscitation failure after 8 or 12 min control hypoxia was a progressive increase in acute cardiac failure. Although magnesium sulfate solution significantly improved immediate recovery after hypoxia (8 and 12 min), mortality due to reperfusion injury (para or tetraplegia) was observed in 62% of rats surviving longer than 1 day after 8 min and 100% after 12 min hypoxia (in control rats-50 and 100%, respectively). The overall survival after hypoxia, with or without reperfusion injury, was relatively low: 28% in control groups after 8 min and 17% after 12 min. In the magnesium sulfate groups these numbers were only slightly higher, 36 and 21%, respectively. It is concluded that in conjunction with arterial reperfusion magnesium sulfate infusion is very effective in improving acute cardiac recovery after 8-12 min of hypoxia. The likely mechanism of magnesium sulfate action is decreased incidence of ventricular fibrillation (VF) and asystole, and possibly myocardial relaxation during and after hypoxia, a property which may qualify MgSO4 as an ischemic preconditioning agent. Poor long-term survival rates of rats exposed to hypoxia and resuscitated by intraarterial reperfusion do not support its use in resuscitation.
本项针对大鼠的研究，调查了体重每千克0.5毫当量/升的硫酸镁溶液对缺氧左心室压力的影响（第1部分）、成功复苏时硫酸镁溶液的最佳注射时机（第2部分），以及在大鼠缺氧8或12分钟后硫酸镁的生存益处（第3部分）。这些大鼠通过单次推注2毫升动脉血和6 - 9微克肾上腺素进行动脉再灌注复苏。总共153只经戊巴比妥麻醉的大鼠接受8或12分钟的0.75%氧气:99.25%氮气缺氧处理，以诱导心脏骤停。在第1部分中，13只大鼠（6只对照，7只注射硫酸镁溶液）接受12分钟缺氧处理，并测量心脏左心室压力（LVP）。在第2部分中，47只大鼠暴露于12分钟缺氧环境。在缺氧前、缺氧2或4分钟时注射生理盐水或硫酸镁溶液，以找到通过动脉再灌注成功复苏的硫酸镁最佳注射时机。在第3部分中，研究90只大鼠以确定7天生存率。两个对照组在缺氧8分钟（29只大鼠）或12分钟（18只大鼠）时注射生理盐水，两个组在缺氧8分钟（14只大鼠）和12分钟（29只大鼠）时接受硫酸镁溶液。硫酸镁完全逆转了缺氧引起的LVP升高，并将缺氧12分钟后的生存率从约15%（对照组）提高到100%，前提是在缺氧的前2.5分钟内给予。在8或12分钟对照缺氧后复苏逐渐失败的主要原因是急性心力衰竭逐渐加重。尽管硫酸镁溶液显著改善了缺氧后（8和12分钟）的即时恢复，但在8分钟缺氧后存活超过1天的大鼠中，62%出现了因再灌注损伤导致的死亡率（截瘫或四肢瘫），12分钟缺氧后这一比例为100%（对照组大鼠分别为50%和100%）。无论有无再灌注损伤，缺氧后的总体生存率相对较低：8分钟后对照组为28%，12分钟后为17%。在硫酸镁组中，这些数字仅略高，分别为36%和21%。结论是，与动脉再灌注联合使用时，硫酸镁输注在改善8 - 12分钟缺氧后的急性心脏恢复方面非常有效。硫酸镁作用的可能机制是降低室颤（VF）和心搏停止的发生率，并且可能在缺氧期间和之后使心肌松弛，这一特性可能使硫酸镁有资格作为一种缺血预处理剂。暴露于缺氧并通过动脉内再灌注复苏的大鼠长期生存率较低，不支持其在复苏中的应用。
