Nimodipine attenuates lipid peroxidation during the acute phase of head trauma in rats
Nimodipine attenuates lipid peroxidation during the acute phase of head trauma in rats
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DOI：
10.1007/pl00012396
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发表时间：
2001-07-01
影响因子：
2.8
通讯作者：
Aypar, Ü
中科院分区：
文献类型：
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作者：
Ercan, M;Inci, S;Aypar, Ü
氧自由基介导的脂质过氧化是创伤性脑损伤继发性损伤的主要机制之一。我们评估了尼莫地平对大鼠头部创伤后 1 小时脂质过氧化的影响。头部外伤后立即通过颈动脉或颈静脉给予尼莫地平（1.5 杯/公斤静脉推注）。安慰剂治疗的大鼠通过相同的途径接受盐水。对照大鼠仅受到头部创伤。假手术大鼠是没有头部外伤的组。丙二醛（MDA）是脂质过氧化的最终产物，被测量为脑组织中氧自由基形成的指标。假手术大鼠的 MDA 平均值为 92.4 +/-4.9 纳摩尔/克脑组织湿重 (nmol/gww)。在对照组中，脑组织的MDA含量为120.8+/-9.4nmol/gww。在安慰剂治疗的大鼠中，结果相似。在通过颈动脉或颈静脉接受尼莫地平的组中，平均值分别为101.1+/-6.9和106.5+/-6.0nmol/gww。这些结果表明，在大鼠头部外伤的急性期给予尼莫地平可导致脂质过氧化显着降低。无论注射途径如何，都会发生这种情况。
Oxygen free radical-mediated lipid peroxidation is one of the major mechanisms of secondary damage in traumatic brain injury. We assessed the effects of nimodipine on lipid peroxidation 1 h after head trauma in rats. Nimodipine (1.5 mug/kg IV bolus injection) was given immediately after head trauma by either the carotid artery or the jugular vein. Placebo treated rats received saline by the same routes. Control rats received head trauma only. Sham-operated rats were the group without head trauma. Malondialdehyde (MDA), which is the end product of lipid peroxidation, was measured as an indicator of oxygen free radical formation in the brain tissue. The mean values for MDA in sham operated rats were 92.4 +/-4.9 nanomoles/gram wet weight (nmol/gww) of brain tissue. In the control group, MDA content of the brain tissue was 120.8 +/-9.4 nmol/gww. In placebo treated rats, the results were similar. In the groups receiving ni modipine via carotid artery or jugular vein, the mean values were 101.1 +/-6.9 and 106.5 +/-6.0 nmol/gww, respectively. These results indicate that nimodipine caused a significant decrease in lipid peroxidation when given in the acute phase of head trauma in rats. This occurred regardless of the route of injection.