• 作者： 曹之憲; C. J. Pfeiffer
• 作者服務機構： 國立陽明醫學院藥理科; 加拿大紐芬蘭大學醫學院
• 中文摘要： 與接受器在使天竺鼠胃及十二指腸潰瘍致病，其所擔當的不同角色已被確定。本實驗特別設計來進一步探討組織胺的致潰瘍性作用及抗組織胺的預防作用（diphenhydramine對接受器及 cimetidine 對接受器）與他們在生體內及試管內對於胃腸及肝臟溶解體脆性的作用之相互關係。 接受器對胃潰瘍的形成（腹腔給藥）及接受器對十二指腸潰瘍的形成（肌肉注射）其關係已被證實。腹腔注射組織胺後有意義的使β-glucuronidase 由胃粘膜組織釋放出來。預處理 diphenhydramine 及 cimetidine 可阻斷這些變化，同時也減少胃潰瘍產生的機會。組織胺也可以增加β-glucuronidase 成不安定狀而由分離出的肝溶解體中釋出，而 diphenhydramine 及 cimetidine 可抑制溶解酵素的釋出。因而推測胃潰瘍的形成與溶解酵素的釋出有關，而此酵素的釋出亦可由組織胺的直接作用於溶解體膜所致。 然而截至目前的研究仍未發現溶解酵素的釋出與十二指腸潰瘍的形成有任何的關連。
• 英文摘要： The differential role of and receptors in the pathogenesis of gastric and duodenal ulcerationin the guinea pig has been established. This study was designed to investigate further the ulcerogenic effectsof histamine and the preventive effect of histamine antagonists (diphenhydramine for receptor, andcimetidine for receptor) in correlation with their actions on gastrointestinal lysosomal fragility in vivo. The involvement of receptors in the formation of gastric ulceration (induced by i.p. injection)and receptors in duodenal ulceration (induced by i.m. injection) was confirmed. Intraperitoneal injection of histamine significantly enhanced β-glucuronidase release from gastricmucosal tissue. This change was blocked by diphenhydramine and cimetidine pretreatment. Concomitant-ly, the incidence of gastric ulceration was reduced. It is suggested that lysosomal enzyme release may bepartially responsible for gastric ulceration and that this enzyme release may be due to the direct or indirectlabilizing action of histamine on lysosomal membranes. However, no correlation has been found betweenlysosomal enzyme release and the formation of duodenal ulcer in the present investigation.
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