论文部分内容阅读
胃酸在消化性溃疡的致病因素中具有重要作用。正常时胃肠上皮细胞间连接紧密,使酸不易逆向扩散。但各种损害使细胞连接处对H~+通透增强,氢离子能通过运载蛋白,穿过细胞的基底侧膜漏入细胞内,从而发生酸化作用。因此,治疗应着眼于降低酸度。近十年来已广泛使用了H_2受体拮抗剂。由于H_2受体在刺激壁细胞分泌胃酸中起着中心作用,其拮抗剂可以阻断绝大部分由胃泌素或毒蕈硷的刺激所致的胃酸分泌。胃粘膜的肠嗜铬样(enterochromaffin—like, ECL)细胞接受胃泌素或乙酰胆硷的刺激而释放组胺。进而组胺刺激H_2受体,激活腺苷环化酶,提高壁细胞内环腺苷酸(cAMP)的水平。cAMP剌激壁细胞使之充分泌酸。目前应用的H_2受体阻滞剂半衰期短,因此,
Gastric acid plays an important role in the pathogenesis of peptic ulcer. Normal gastrointestinal epithelial cells are closely connected, so that the acid is not easy to reverse diffusion. However, various damage to the cell junction H ~ + permeability increased, hydrogen ions through the carrier protein, through the basolateral membrane cells leak into the cell, resulting in acidification. Therefore, treatment should focus on reducing acidity. Over the past decade has been widely used H 2 receptor antagonist. Since H 2 receptors play a central role in stimulating the secretion of gastric acid by parietal cells, their antagonists block the gastric acid secretion, which is mostly caused by the stimulation of gastrin or muscarinic. Gastric mucosal enterochromaffin-like (ECL) cells are stimulated by gastrin or acetylcholine to release histamine. Histamine then stimulates H 2 receptors, activates adenylyl cyclase, and increases intracellular adenylate (cAMP) levels in parietal cells. CAMP stimulates parietal cells to make full acid secretion. The current application of H 2 receptor blockers short half-life, therefore,