Post resuscitation iron delocalization and malondialdehyde production in the brain following prolonged cardiac arrest

Narsimha R. Nayini Ph.D. , Blaine C. White M.D. , Steven D. Aust Ph.D. , Raywin R. Huang Ph.D. , Richard J. Indrieri D.V.M. , A.Thomas Evans D.V.M. , Howard Bialek M.D. , William A. Jacobs M.D. , James Komara D.O.
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引用次数: 78

Abstract

Assays for brain tissue malondialdehyde (MDA) and low molecular weight chelated (LMWC) iron were used to examine samples of the cerebral cortex obtained from dogs 2 h after resuscitation from a 15-min cardiac arrest. The effect of post-resuscitation treatment with lidoflazine and/or desferrioxamine was similarly examined. Non-ischemic brain samples had LMWC iron levels (in nmol/100 mg tissue) of 12.32 + 2.60 and MDA levels (in nmol/100 mg tissue) of 8.46 + 1.35. Animals subjected to cardiac arrest and resuscitation and standard intensive care (SIC) had LMWC iron levels of 37.04 +_4.58 (p < .01 against non-ischemic controls) and MDA levels of 12.24 + 1.9 (p < .05 against non-ischemic controls). All treatment interventions significantly reduced the LMWC iron (p < .05), but only treatment with desferrioxamine alone significantly reduced MDA (p < .05), although a trend toward reduction of the MDA was also evident in animals treated with both desferrioxamine and lidoflazine. LMWC iron levels are increased in the post-ischemic brain, and this increase may be related to lipid peroxidation in the brain following resuscitation from cardiac arrest. These changes are probably pathologic and are amenable to pharmacologic intervention.

长时间心脏骤停后复苏后脑内铁的脱位和丙二醛的产生
采用脑组织丙二醛(MDA)和低分子量螯合铁(LMWC)的检测方法,对心脏骤停15分钟复苏后2小时的大脑皮层样本进行检测。复苏后使用利多氟嗪和/或去铁胺治疗的效果也进行了类似的检查。非缺血性脑样品的低分子碳水化合物铁水平(nmol/100 mg组织)为12.32 + 2.60,MDA水平(nmol/100 mg组织)为8.46 + 1.35。接受心脏骤停和复苏和标准重症监护(SIC)的动物的LMWC铁水平为37.04 + 4.58 (p <与非缺血性对照组相比,MDA水平为12.24 + 1.9 (p <非缺血性对照组0.05)。所有治疗干预措施均显著降低了低分子wc铁(p <.05),但仅单独使用去铁胺可显著降低丙二醛(p <.05),尽管在用去铁胺和利多嗪治疗的动物中,丙二醛的降低趋势也很明显。脑缺血后LMWC铁水平升高,这种升高可能与心脏骤停复苏后脑脂质过氧化有关。这些变化可能是病理性的,可以进行药物干预。
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