Role of bile acid reflux in acute hemorrhagic gastritis
Role of bile acid reflux in acute hemorrhagic gastritis
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胆汁酸反流在急性出血性胃炎中的作用
DOI：
10.1007/bf01658286
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发表时间：
1981
影响因子：
2.6
通讯作者：
W. Ritchie
中科院分区：
文献类型：
--
作者：
W. Ritchie
建立了胆汁酸对犬近端胃粘膜维持管腔内pH梯度和抵抗急性形态损伤能力的影响模型。研究发现，局部酸、局部胆汁酸和粘膜缺血的组合是急性和严重的溃疡形成。病变严重程度是H+绝对量的函数；扩散到粘膜本身是胆汁和H+腔内浓度的函数。形态损伤与明显的胃静脉酸中毒的发展有关。胆汁酸种类不同，其诱发损伤的能力也不同。局部应用胆汁酸到非缺血粘膜并不是急性溃疡，因为粘膜血流量的代偿性增加与引起H+丢失的程度成正比。在目前的模型中，类固醇通过这种机制具有“细胞保护”作用，而组胺H1和H2受体拮抗剂，无论是顺着还是结合在一起，都不具有细胞保护作用。对这些发现的临床适用性进行了讨论。
A model was developed to assess the influence of bile acids on the ability of proximal canine gastric mucosa to maintain an intraluminal pH gradient and to resist acute morphologic injury. It was found that the combination of topical acid, topical bile acid, and mucosal ischemia is acutely and severely ulcerogenic. Lesion severity is a function of the absolute amount of H+; diffusing into the mucosa which is, itself, a function of the intraluminal concentrations of both bile and H+. Morphologic injury is associated with the development of a marked gastric venous acidosis. Bile acid species differ in their capacity to induce lesions. Topical application of bile acids to nonischemic mucosa is not acutely ulcerogenic because a compensatory increase in mucosal blood flow occurs which is proportional to the degree of H+loss induced. In the present model, steroids are “cytoprotective” by virtue of this mechanism, while histamine H1and H2receptor antagonists, either along or in combination, are not. The clinical applicability of these findings is discussed.