Kompala S D, Babbs C F, Blaho K E
Ann Emerg Med. 1986 Apr;15(4):405-7. doi: 10.1016/s0196-0644(86)80175-5.
The iron-chelating agent deferoxamine was studied in an animal model as postresuscitation therapy to prevent late deaths and brain damage following total circulatory arrest and resuscitation. Cardiorespiratory arrest was induced by injection of cold, 1% KCl into the left ventricles of ketamine-anesthetized rats pretreated with succinylcholine, and by discontinuation of positive pressure ventilation. CPR was begun after six minutes, and animals with return of spontaneous circulation were entered into the study. Within five minutes after return of spontaneous circulation, treated animals received deferoxamine (50 mg/kg, IV). At ten days, 16 of 25 (64%) of treated animals had survived without neurologic deficit, compared to nine of 25 (36%) of controls (chi square = 3.92, P less than .05). Chelation of intracellular iron by deferoxamine may have prevented free-radical-mediated reactions that led to late deaths in control animals.
在动物模型中研究了铁螯合剂去铁胺作为复苏后治疗手段，以预防全循环骤停和复苏后的晚期死亡及脑损伤。通过向预先用琥珀酰胆碱处理的氯胺酮麻醉大鼠的左心室注射冷的1%氯化钾并停止正压通气来诱导心肺骤停。六分钟后开始进行心肺复苏，恢复自主循环的动物进入研究。在恢复自主循环后五分钟内，治疗组动物接受去铁胺（50mg/kg，静脉注射）。十天时，25只治疗组动物中有16只（64%）存活且无神经功能缺损，而对照组25只中有9只（36%）存活（卡方检验=3.92，P<0.05）。去铁胺对细胞内铁的螯合作用可能预防了导致对照组动物晚期死亡的自由基介导反应。
