颅脑创伤早期兴奋性氨基酸的变化及其意义

目的探讨兴奋性氨基酸（ＥＡＡ）在颅脑创伤早期的变化及钙通道阻断剂治疗外伤性脑水肿的机制。方法通过大鼠脑外伤模型检测了外伤后脑组织含水率、脑脊液中ＥＡＡ含量以及钙通道阻断剂（尼莫地平）对两者变化的影响；通过神经细胞培养模型观察了钙通道激动剂（Ｂａｙ－Ｋ－８６４４）、谷氨酸（Ｇｌｕ）、天门冬氨酸（Ａｓｐ）及尼莫地平对神经元钙通道电流（ＩＣａ）的影响。结果外伤后脑组织含水率、脑脊液ＥＡＡ含量均较对照组明显增加（Ｐ＜０．０５），用尼莫地平治疗后两者均明显下降（Ｐ＜０．０５）。Ｂａｙ－Ｋ－８６４４、Ｇｌｕ、Ａｓｐ可使培养神经元ＩＣａ增加，并存在明显的剂量依赖关系。结论颅脑创伤早期ＥＡＡ释放增加，ＥＡＡ促进Ｃａ２＋内流。钙通道阻断剂治疗外伤性脑水肿的机制是抑制脑外伤后ＥＡＡ释放及直接减少Ｃａ２＋内流。

Alteration and Significance of Excitatory Amino Acid at Early Stage of Traumatic Brain Injury

Aim To study the alteration of excitatory amino acid (EAA) at the early stage of traumatic brain injury and to explore the mechanism of treating traumatic cerebral edema with calcium channel blocker. Methods The water content, EAA in the cerebrospinal fluid (CSF) were measured after brain injury. The effect of calcium channel blocker (nimodipine) on the water content and EAA was observed, and the effect of calcium agonist (Bay K 8644), glutamate, aspartate and nimodipine on calcium currents (I Ca ) in cultured cortical neurons was also studied. Results It showed that the water content and EAA increased after brain injury. This increase could be inhibited by nimodipine. I Ca was raised dose dependently by Bay K 8644, glutamate and aspartate, and reduced by nimodipine. Conclusions EAA releasing can increase at the early stage of traumatic brain injury. Ca 2 influx is raised by EAA. The mechanism of treating traumatic cerebral edema with calcium channel blocker is to inhibit EAA releasing and to inhibit Ca 2 influx directly.