The role of the monosialoganglioside, GM1, as a neuroprotectant in an experimental model of cardiopulmonary bypass and hypothermic circulatory arrest
The role of the monosialoganglioside, GM1, as a neuroprotectant in an experimental model of cardiopulmonary bypass and hypothermic circulatory arrest
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DOI：
10.1111/j.1749-6632.1998.tb09690.x
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发表时间：
1998-01-01
期刊：
影响因子：
--
通讯作者：
Johnston, MV
中科院分区：
文献类型：
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作者：
Baumgartner, WA;Redmond, JM;Johnston, MV
将 12 只雄性狗置于闭胸体外循环中，在 18 摄氏度下进行 2 小时的 HCA，并在闭胸体外循环中复温至 37 摄氏度。所有动物在拔管前均进行机械通气并监测20小时，并存活3天。第1组狗（n = 6）在HCA前用GM（1）30 mg/kg/24小时预处理3天，并在手术过程中持续输注GM（1），并在HCA后接受30 mg/kg/24小时连续输注3天。第 2 组狗（n=6）仅接受车辆。根据物种特异性行为量表，神经缺陷评分范围从 0%（正常）到 100%（脑死亡），两名观察者每 12 小时对所有动物进行一次神经学评估。 72小时死亡后，通过谷氨酸受体放射自显影和组织学检查来检查大脑的选择性神经元坏死模式，并从0（正常）到100（严重损伤）进行盲法评分。这些结果提供了 GE 在 HCA 诱导的脑损伤发展中的作用的证据，并表明单唾液酸神经节苷脂可能在长时间的 HCA 中具有神经保护作用。
Twelve male dogs were placed on closed-chest cardiopulmonary bypass, subjected to 2 h of HCA at 18 degrees C, and rewarmed to 37 degrees C on closed-chest cardiopulmonary bypass. All animals were mechanically ventilated and monitored for 20 h before extubation and survived for 3 days. Group 1 dogs (n=6) were pretreated with GM(1), 30 mg/kg/24 h for 3 days before HCA, and received continuous infusion of GM(1) during the procedure and 30 mg/kg/24 h for 3 days after HCA. Group 2 dogs (n=6) received vehicle only. With a species-specific behavior scale that yielded a neurodeficit score ranging from 0% (normal) to 100% (brain dead), all animals were neurologically assessed every 12 h by two observers. After death at 72 h, brains were examined by glutamate receptor autoradiography and by histologic examination for patterns of selective neuronal necrosis and were scored blindly from 0 (normal) to 100 (severe injury). These results provide evidence of a role for GE in the development of HCA-induced brain injury and suggest that monosialogangliosides may have a neuroprotective effect in prolonged periods of HCA.