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目的研究大鼠冷冻伤性脑水肿不同时间脑组织伊文思兰（ＥＢ）、突触体内［Ｃａ２＋］ｉ及Ｃａ２＋－ＡＴＰ酶活性变化与脑含水量变化之间的规律，以探讨冷冻伤性脑水肿的发生机制和类型。方法干湿法测定脑组织水分含量，甲酰胺法测定ＥＢ含量，Ｆｕｒａ－２／ＡＭ荧光标记法测定突触体内［Ｃａ２＋］ｉ，微量定磷法测定线粒体Ｃａ２＋－ＡＴＰ酶活性。采用尼莫地平进行治疗，研究其对ＥＢ含量、［Ｃａ２＋］ｉ、Ｃａ２＋－ＡＴＰ酶活性和脑水肿的影响。结果冷冻伤后３０分钟即已发生Ｃａ２＋超载，伴随Ｃａ２＋－ＡＴＰ酶活性下降及脑组织水分含量及ＥＢ含量增加。尼莫地平治疗后ＥＢ含量和［Ｃａ２＋］ｉ明显下降，而Ｃａ２＋－ＡＴＰ酶活性明显恢复，脑水肿明显减轻。结论ＢＢＢ的通透性增加和细胞内钙通道开放，钙离子浓度超载在脑水肿的发生与发展过程中起了重要作用。冷冻伤性脑水肿在早期既有细胞毒性脑水肿，又有血管源性脑水肿，即混合性脑水肿。
OBJECTIVE: To study the regularity of the changes of brain edema (EB), synaptic [Ca2 +] i and Ca2 + -ATPase activity and brain water content in rats with cold-induced brain edema at different time points, The mechanism and type of edema. Methods Moisture content of brain tissue was determined by wet and dry method. EB content was determined by formamide method. [Ca2 +] i in synaptosome was measured by Fura-2 / AM fluorescence method and mitochondrial Ca2 + -ATPase activity was measured by micro-determination of phosphorus. Nimodipine was used to study its effects on EB content, [Ca2 +] i, Ca2 + -ATPase activity and brain edema. Results Ca2 + overloading occurred 30 minutes after the injury in the cold injury, accompanied by decreased Ca2 + -ATPase activity and increased brain water content and EB content. After nimodipine treatment EB content and [Ca2 +] i decreased significantly, while Ca2 + -ATP enzyme activity was significantly recovered, brain edema significantly reduced. Conclusion The increased permeability of BBB and the opening of intracellular calcium channels play an important role in the occurrence and development of cerebral edema. Cold injury of cerebral edema in both early cytotoxic brain edema, and angiogenic brain edema, that is, mixed brain edema.