Huber T S, Nachreiner R, D'Alecy L G
Department of Physiology, University of Michigan Medical School, Ann Arbor 48109-0622.
J Crit Care. 1994 Mar;9(1):7-17. doi: 10.1016/0883-9441(94)90028-0.
The aim of the present study was to determine the effect of brain death on the circulating hormone levels.
Serum total thyroxine (TT4), total 3,3,5' triiodothyronine (TT3), free thyroxine (FT4), free 3,3,5' triiodothyronine (FT3), reverse 3,3',5' triiodothyronine (RT3) and plasma cortisol (CORT), norepinephrine (NE), epinephrine (EPI), dopamine, insulin (INS), and glucagon (GLUC) concentrations were measured before and for 5 hours after the maintenance of brain death (BD, n = 8), sham-brain death induction (SHAM, n = 3), and the operative procedure alone (time control, n = 3). Brain death in the canine model was induced by increasing and maintaining intracranial pressure above systolic arterial pressure.
Brain death led to a persistent, significant decrease in mean arterial pressure (121 +/- 6 v 40 +/- 4 mm Hg at 5 hours). A significant decrease in the TT4, TT3, FT4, and FT3 concentrations was seen during the experiment for all three groups with the exception of TT4 in the SHAM group; no significant difference was found among the three groups for any of the time points. RT3 was found to increase after the induction of brain death in the BD (n = 5) group. The CORT levels in the BD group were significantly less than the other two groups for all time points 30 minutes after the induction of brain death. The mean 30- to 300-minute plasma NE and EPI levels in the SHAM group were statistically greater than the BD group. The plasma glucose in the BD group was maintained between 60 and 140 mg/dL whereas the trends of the INS/glucose and GLUC/glucose ratios in the BD group were appropriate for the plasma glucose level.
The operative procedure alone led to the decrease in the plasma thyroid hormone levels. The inability of the BD group to increase plasma CORT, NE, and EPI may contribute to the hemodynamic deterioration and eventual somatic death.
本研究旨在确定脑死亡对循环激素水平的影响。
在维持脑死亡（BD，n = 8）、假脑死亡诱导（SHAM，n = 3）以及仅进行手术操作（时间对照，n = 3）之前及之后5小时，测量血清总甲状腺素（TT4）、总三碘甲状腺原氨酸（TT3）、游离甲状腺素（FT4）、游离三碘甲状腺原氨酸（FT3）、反三碘甲状腺原氨酸（RT3）以及血浆皮质醇（CORT）、去甲肾上腺素（NE）、肾上腺素（EPI）、多巴胺、胰岛素（INS）和胰高血糖素（GLUC）的浓度。犬模型中的脑死亡通过将颅内压升高并维持在收缩动脉压以上来诱导。
脑死亡导致平均动脉压持续显著下降（5小时时为121±6 vs 40±4 mmHg）。在实验期间，所有三组的TT4、TT3、FT4和FT3浓度均显著下降，但SHAM组的TT4除外；在任何时间点，三组之间均未发现显著差异。发现BD组（n = 5）在脑死亡诱导后RT3升高。在脑死亡诱导后30分钟的所有时间点，BD组的CORT水平均显著低于其他两组。SHAM组血浆NE和EPI的平均30至300分钟水平在统计学上高于BD组。BD组的血浆葡萄糖维持在60至140 mg/dL之间，而BD组的INS/葡萄糖和GLUC/葡萄糖比值趋势与血浆葡萄糖水平相符。
仅手术操作导致血浆甲状腺激素水平下降。BD组无法增加血浆CORT、NE和EPI可能导致血流动力学恶化及最终的躯体死亡。
