肾上腺切除术增强了清醒大鼠肿瘤坏死因子-α（TNF-α）对出血的反应。
Adrenalectomy enhances response of tumour necrosis factor-alpha (TNF-alpha) to haemorrhage in the conscious rat.
作者信息
Yamashita M, Yamashita M
机构信息
Department of Emergency Medicine, University of Tsukuba School of Medicine, Tsukuba, Japan.
出版信息
Clin Exp Immunol. 2001 Jan;123(1):23-7. doi: 10.1046/j.1365-2249.2001.01444.x.
Several factors have been implicated in TNF-alpha induction after haemorrhage, but the precise mechanism is unknown. To assess a possible role of adrenal glands on TNF-alpha induction after haemorrhage, adrenalectomized (ADX) and sham-adrenalectomized (Sham) rats were subjected to 20 ml/kg haemorrhage (approximately 30% of the total blood volume) over 5 min in the conscious state, and changes in serum TNF and hepatic TNF-alpha mRNA were analysed by cytotoxicity against L929 cells and by semiquantitative reverse transcription-polymerase chain reaction, respectively. Changes in plasma corticosterone (CS) and mean arterial blood pressure (MABP) were also detected. Plasma CS levels showed a rapid increase after haemorrhage in Sham rats, whereas there was no response in ADX rats. Responses of MABP were comparable in the two groups. Both serum TNF and hepatic TNF-alpha mRNA showed rapid increases after haemorrhage in the Sham group, and these increases were significantly augmented in the ADX group. Pretreatment with CS (100 microg/h) negated these augmentations in ADX rats. These results show that adrenalectomy enhances the response of TNF-alpha to 20 ml/kg haemorrhage in the conscious rat, and suggest that endogenous glucocorticoids may play an inhibitory role in the induction of TNF-alpha after haemorrhage.
出血后肿瘤坏死因子-α（TNF-α）的诱导涉及多种因素，但确切机制尚不清楚。为了评估肾上腺在出血后TNF-α诱导中的可能作用，将肾上腺切除（ADX）和假肾上腺切除（Sham）大鼠在清醒状态下于5分钟内进行20 ml/kg出血（约占总血容量的30%），并分别通过对L929细胞的细胞毒性和半定量逆转录-聚合酶链反应分析血清TNF和肝脏TNF-α mRNA的变化。还检测了血浆皮质酮（CS）和平均动脉血压（MABP）的变化。Sham大鼠出血后血浆CS水平迅速升高，而ADX大鼠无反应。两组MABP的反应相当。Sham组出血后血清TNF和肝脏TNF-α mRNA均迅速升高，且ADX组的这些升高显著增强。用CS（100μg/h）预处理可消除ADX大鼠中的这些增强作用。这些结果表明，肾上腺切除术增强了清醒大鼠对20 ml/kg出血时TNF-α的反应，并提示内源性糖皮质激素可能在出血后TNF-α的诱导中起抑制作用。
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