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[交感肾上腺髓质系统对自发性高血压大鼠(SHR)和正常血压Wistar-Kyoto大鼠(WKY)中半胱胺诱导的胃溃疡的抑制作用]

[Inhibition of the cysteamine-induced gastric ulcer by the sympathoadrenal medullary system in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY)].

作者信息

Shikuwa S

机构信息

Department of Pathology, Atomic Disease Institute, Nagasaki University School of Medicine.

出版信息

Nihon Shokakibyo Gakkai Zasshi. 1991 Oct;88(10):2627-35.

PMID:1758079
Abstract

We previously reported that cysteamine induces severe gastric ulcers in WKY, but very mild in SHR. The aim of this study is to elucidate the role on the sympathoadrenal medullary system in the pathogenesis of the cysteamine-induced gastric ulcer. Catecholamine (CA) contents in the stomach and adrenal gland were significantly higher in the non-treated SHR than in the non-treated WKY, suggesting that the sympathetic nervous system is more facilitated in SHR. Cysteamine decreased the noradrenaline and adrenaline contents in these tissues in both strains, however the values of CA was still higher in the treated SHR than the non-treated WKY. Histologically the adrenal medulla was severely damaged by cysteamine administration in WKY than in SHR. In contrast an immunohistological study revealed that chromogranin reactivity of the adrenal medulla was significantly stronger in the treated SHR than in the treated WKY. The celiac plexus was well preserved morphologically even in the cysteamine treatment in both strains. These results suggest that the capacity of the sympathetic nervous system in both the adrenal medulla and the stomach plays an important role in preventing the cysteamine-induced gastric ulcer in SHR.

摘要

我们之前报道过,半胱胺可在WKY大鼠中诱发严重胃溃疡,但在SHR大鼠中诱发的胃溃疡则非常轻微。本研究的目的是阐明交感肾上腺髓质系统在半胱胺诱发胃溃疡发病机制中的作用。未处理的SHR大鼠胃和肾上腺中的儿茶酚胺(CA)含量显著高于未处理的WKY大鼠,这表明SHR大鼠的交感神经系统更易兴奋。半胱胺降低了两种品系大鼠这些组织中的去甲肾上腺素和肾上腺素含量,然而,处理后的SHR大鼠的CA值仍高于未处理的WKY大鼠。组织学上,与SHR大鼠相比,WKY大鼠经半胱胺给药后肾上腺髓质受到的损伤更严重。相反,一项免疫组织学研究显示,处理后的SHR大鼠肾上腺髓质嗜铬粒蛋白反应性明显强于处理后的WKY大鼠。即使在两种品系大鼠经半胱胺处理后,腹腔神经丛在形态上仍保存完好。这些结果表明,肾上腺髓质和胃中交感神经系统的功能在预防SHR大鼠半胱胺诱发的胃溃疡中起重要作用。

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