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创伤性出血后男性免疫抑制的机制。睾酮的关键作用。

Mechanism of immunosuppression in males following trauma-hemorrhage. Critical role of testosterone.

作者信息

Wichmann M W, Zellweger R, DeMaso C M, Ayala A, Chaudry I H

机构信息

Department of Surgery, Michigan State University, East Lansing, USA.

出版信息

Arch Surg. 1996 Nov;131(11):1186-91; discussion 1191-2. doi: 10.1001/archsurg.1996.01430230068012.

DOI:10.1001/archsurg.1996.01430230068012
PMID:8911259
Abstract

OBJECTIVE

To determine whether male sex steroids contribute to the depression in cell-mediated immunity following trauma-hemorrhage and resuscitation.

DESIGN

Two weeks before the induction of soft-tissue trauma (2.5-cm midline laparotomy) and hemorrhagic shock (mean [+/-SEM] blood pressure, 35 +/- 5 mm Hg), male C3H/HeN mice were castrated or sham castrated. Following trauma-hemorrhage, the mice were resuscitated and killed 24 hours thereafter to obtain whole blood and the spleen.

RESULTS

Splenocyte proliferation and splenocyte interleukin-2 and interleukin-3 release were significantly depressed in sham-castrated animals after trauma-hemorrhage. In contrast, these variables in castrated mice after trauma-hemorrhage were similar to those in sham-operated animals. Corticosterone plasma levels were significantly elevated in both trauma-hemorrhage groups compared with those in sham-operated mice. Plasma testosterone levels were undetectable in castrated animals and detectable in sham-castrated mice.

CONCLUSIONS

Castration before soft-tissue trauma and hemorrhagic shock maintains normal immune function in male mice, but sham-castrated male mice show significant immunodepression. The maintenance of immune function by androgen deficiency does not seem to be related to changes in the release of corticosterone. We conclude that male sex steroids are involved in the immunodepression observed after trauma-hemorrhage. Thus, the use of testosterone-blocking agents following trauma-hemorrhage should prevent the depression of immune functions and decrease the susceptibility to sepsis under those conditions.

摘要

目的

确定男性甾体激素是否会导致创伤性出血及复苏后细胞介导免疫功能的抑制。

设计

在诱导软组织创伤(2.5厘米中线剖腹术)和失血性休克(平均[±标准误]血压,35±5毫米汞柱)前两周,对雄性C3H/HeN小鼠进行去势或假去势手术。创伤性出血后,对小鼠进行复苏,并在24小时后处死以获取全血和脾脏。

结果

创伤性出血后,假去势动物的脾细胞增殖以及脾细胞白细胞介素-2和白细胞介素-3的释放均显著受到抑制。相比之下,创伤性出血后去势小鼠的这些指标与假手术动物相似。与假手术小鼠相比,两个创伤性出血组的血浆皮质酮水平均显著升高。去势动物血浆睾酮水平检测不到,而假去势小鼠可检测到。

结论

在软组织创伤和失血性休克前进行去势可维持雄性小鼠的正常免疫功能,但假去势雄性小鼠表现出显著的免疫抑制。雄激素缺乏对免疫功能的维持似乎与皮质酮释放的变化无关。我们得出结论,男性甾体激素参与了创伤性出血后观察到的免疫抑制。因此,创伤性出血后使用睾酮阻断剂应可预防免疫功能抑制,并降低在这些情况下发生脓毒症的易感性。

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Mechanism of immunosuppression in males following trauma-hemorrhage. Critical role of testosterone.创伤性出血后男性免疫抑制的机制。睾酮的关键作用。
Arch Surg. 1996 Nov;131(11):1186-91; discussion 1191-2. doi: 10.1001/archsurg.1996.01430230068012.
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