Atrakchi A H, Bloom S, Dickens B F, Mak I T, Weglicki W B
Division of Experimental Medicine, The George Washington Medical Center, Washington, D.C., USA.
Department of Pathology, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Cardiovasc Pathol. 1992 Apr-Jun;1(2):155-60. doi: 10.1016/1054-8807(92)90019-K.
Chronic magnesium deficiency is associated with injury of heart muscle, blood vessels, and neuronal tissue. Despite its clinical significance, the mechanism of magnesium deficiency-induced damage remains unclear. The myocardial necrosis induced by injecting catecholamines, which is augmented by magnesium deficiency, is thought to involve a free radical component through catecholamine autoxidation. α-tocopherol was shown to ameliorate the myocardial necrosis induced by magnesium-deficiency (Freedman et al. BBRC 1990;170:1102-1106), suggesting a role for free radicals in this process. If free-radical injury plays a role in magnesium deficiency, then the catecholamine-associated free-radical production may explain the synergistic myocardial injury between catecholamine and magnesium deficiency. To test the hypothesis that free-radical damage may play a role in magnesium deficiency-induced myocardial necrosis, we investigated the protective effects of probucol, a hypolipidemic agent with antioxidant properties. Hamsters were fed a Mg-deficient diet for 14 days with or without probucol. At the end of this period, some animals were sacrificed, while others were injected with isoproterenol and killed 48 hours later. All hearts were processed for morphometric analysis of the lesions. Changes in serum lipids were also determined. Probucol reduced the size and number of both the isoproterenol- and magnesium deficiency-induced cardiac lesions. Our results suggest that it is probucol's antioxidant property and not its hypolipidemic action that is responsible for this protection.
慢性镁缺乏与心肌、血管和神经组织损伤有关。尽管其具有临床意义，但镁缺乏所致损伤的机制仍不清楚。注射儿茶酚胺诱导的心肌坏死在镁缺乏时会加重，这被认为是通过儿茶酚胺自氧化涉及自由基成分。已表明α-生育酚可改善镁缺乏诱导的心肌坏死（Freedman等人，《生物化学与生物物理研究通讯》1990年；170:1102 - 1106），提示自由基在此过程中起作用。如果自由基损伤在镁缺乏中起作用，那么儿茶酚胺相关的自由基产生可能解释了儿茶酚胺与镁缺乏之间的协同心肌损伤。为了检验自由基损伤可能在镁缺乏诱导的心肌坏死中起作用这一假说，我们研究了普罗布考（一种具有抗氧化特性的降血脂药物）的保护作用。仓鼠喂食缺镁饮食14天，同时给予或不给予普罗布考。在此期间结束时，处死一些动物，而其他动物注射异丙肾上腺素并在48小时后处死。所有心脏均进行病变的形态计量分析。还测定了血脂变化。普罗布考减少了异丙肾上腺素和镁缺乏诱导的心脏病变的大小和数量。我们的结果表明，起这种保护作用的是普罗布考的抗氧化特性而非其降血脂作用。
