重症急性脑损伤过程中尿儿茶酚胺排泄及血甲状腺激素水平的变化。

W Haider, H Benzer, G Krystof, F Lackner, O Mayrhofer, K Steinbereithner, K Irsigler, A Korn, W Schlick, H Binder, F Gerstenbrand
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引用次数: 15

摘要

对16例重型颅脑外伤患者的尿儿茶酚胺排泄及血甲状腺激素水平进行了研究。肾上腺素和去甲肾上腺素的排泄率增加。与一般创伤患者相比,儿茶酚胺排泄无显著差异。儿茶酚胺排泄、代谢率增加和负氮平衡之间的关系表明,中脑综合征患者存在额外的间脑代谢因子,导致脂肪氧化增加和分解代谢持续存在。早期的高热量肠外营养似乎抑制了儿茶酚胺排泄的初始增加,从而保护身体免受自身储备的不必要破坏。如果将病程按神经学分期进行分类,可以看出,病情较差的外伤性阴虚综合征患者儿茶酚胺排泄量增高。甲状腺激素的分泌不受脑外伤的显著影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Urinary catecholamine excretion and thyroid hormone blood level in the course of severe acute brain damage.

Urinary catecholamine excretion and thyroid hormone blood level were studied in 16 patients following severe cerebral trauma. Increased excretion rates of epinephrine and norepinephrine were found. There was no significant difference in the catecholamine excretion when compared with generally traumatized patients. The relationships between catecholamine excretion, increased metabolic rates, and negative nitrogen balance indicate that in patients with a midbrain syndrome there exists an additional diencephalic metabolic factor, which leads to a rise in fat oxidation and perpetuation of catabolism. Early high caloric parenteral nutrition seems to inhibit the initial increase of catecholamine excretion and thus protects the body from an unnecessary breakdown of its own reserves. If the course is classified according to neurological stages, it can be shown that patients with a traumatic apallic syndrome in poor condition have a high increase of catecholamine excretion. Secretion of thyroid hormones is not influenced significantly by cerebral trauma.

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