エタノールによるラット胃粘膜病変発生におけるエンドセリンー1の病因的役割
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概要
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The pathogenetic role of endothelin-1 (ET-1), which is a potent vasoconstrictor peptide derived from vascular endothelial cells, was studied using a model of ethanol (EtOH)-induced gastric mucosal damage (GMD) in the rat. Synthetic peptide ET-1 infusion into the left gastric artery caused mucosal alterations such as edema, erythema and erosion and, microscopically, marked dilatation and congestion of collecting venules in the lamina propria mucosae. Inasmuch as monastral blue B pigments, a vascular tracer, were deposited remarkably in the lamina propria mucosae, it was strongly suggested that ET-1 directly gave rise to mucosal vascular damage. ET-1 reduced gastric mucosal blood flow in a dosedependent manner and significantly increased the lesion score of gastric mucosa. After ingestion of 50% EtOH, immunohistological examination showed that endogenous ET-1 occurred in the vascular endothelial cells in the deep parts of fundic glands. In addition, it was confirmed using immunoblot analysis that monoclonal anti-ET-1 antibody reacted to the extracts of fundic mucosa from rats treated with 50% EtOH ingestion. Infusion of anti-ET-1 serum (1:500) into the jugular vein significantly depressed the development of GMD induced by 50% EtOH ingestion, while pooled normal rabbit serum (1:500) infusion did not. Low concentrations of EtOH stimulated immunoreactive ET-1 release from a cultured cell of human vascular endothelium, but did not release 6-keto-PGF?a, a PGI? metabolic product. These results strongly suggest that endogenous ET-1 is released from vascular endothelial cells in the fundic mucosa by EtOH ingestion and may have an important role in the pathogenesis of EtOH-induced GMD.
- 札幌医科大学の論文
- 1993-08-01
札幌医科大学 | 論文
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