Bech K
Institute of Surgery, Odense University Hospital.
Dan Med Bull. 1988 Apr;35(2):122-40.
CHAPTER 1. The gastric functions are regulated in a complex manner by the autonomic nervous system, sympathetic and parasympathetic, and hormones and moreover by a system of peptide-containing cells and nerves. The sympathetic influence is mediated by alpha- and beta-adrenoceptors, beta-adrenoceptor agonists in general inhibit the gastric functions. The effects of the beta-adrenoceptors are probably mediated indirectly, and the responsible mechanism may be via release of and endogenous mediator--somatostatin or serotonin. The purpose of the present study, described in the survey, is to examine whether somatostatin or serotonin acts as a mediator for the gastric effects in vivo of beta-adrenoceptor agonists. The proposed mediator must present the following characteristics: A. Inhibitory effects of "physiological" doses in vivo. B. Inhibitory characteristics similar to those of the beta-adrenoceptor agonists. C. A beta-adrenoceptor mediated release. CHAPTER 2. In this chapter the known effects of beta-adrenoceptor agonists on gastric functions (acid secretion, pepsin secretion, antral motility and mucosal blood flow) are presented. The possible mechanisms mediating these effects are mentioned, and the effects of somatostatin and serotonin are reviewed. Beta-adrenoceptor agonists inhibit the acid secretion in vivo in several species, but stimulate in vitro. A similar pattern is probable as for the pepsin secretion, but sufficient results are not available in order to draw a certain conclusion. The antral motility is inhibited both in vivo and in vitro. The mucosal blood flow is increased compared to the acid secretion, however the results points to variable effects depending on the circumstances of the experiments. On the basis of the reviewed effects of somatostatin it is concluded that the effects are inhibitory, but the inhibitory characteristics are not known. A beta-adrenoceptor mediated release of somatostatin has been found, but it has not been examined selectively for the stomach. The gastric effects of serotonin has been sparsely examined and it is not possible to determine the effects as parts of a certain characteristic. It is concluded that neither somatostatin nor serotonin have been examined sufficiently to determine which is the proposed mediator. CHAPTER 3. The materials and methods used are reviewed. Dogs were used and various parameters were measured--acid secretion by titration, pepsin secretion by enzymatic process with haemoglobin as substrate, antral motility by registration of intraluminal pressure, mucosal blood flow by the clearance of neutral red, somatostatin by radioimmunoassay.(ABSTRACT TRUNCATED AT 400 WORDS)
第1章。胃功能由自主神经系统（交感神经和副交感神经）、激素，以及一个含肽细胞和神经的系统以复杂的方式进行调节。交感神经的影响是通过α和β肾上腺素能受体介导的，一般来说β肾上腺素能受体激动剂会抑制胃功能。β肾上腺素能受体的作用可能是间接介导的，其相关机制可能是通过释放一种内源性介质——生长抑素或血清素。本研究（在综述中描述）的目的是检验生长抑素或血清素是否作为β肾上腺素能受体激动剂在体内对胃产生作用的介质。所提出的介质必须具备以下特征：A. 在体内“生理”剂量下具有抑制作用。B. 具有与β肾上腺素能受体激动剂相似的抑制特征。C. 由β肾上腺素能受体介导释放。第2章。本章介绍了β肾上腺素能受体激动剂对胃功能（胃酸分泌、胃蛋白酶分泌、胃窦运动和黏膜血流量）的已知作用。提及了介导这些作用的可能机制，并综述了生长抑素和血清素的作用。β肾上腺素能受体激动剂在体内抑制多种物种的胃酸分泌，但在体外则起刺激作用。胃蛋白酶分泌可能也有类似模式，但尚无足够结果得出确切结论。胃窦运动在体内和体外均受到抑制。与胃酸分泌相比，黏膜血流量增加，然而结果表明根据实验情况其作用存在差异。基于对生长抑素作用的综述得出结论，其作用是抑制性的，但抑制特征尚不清楚。已发现生长抑素由β肾上腺素能受体介导释放，但尚未针对胃进行选择性研究。血清素对胃的作用研究较少，无法确定其作为某种特定特征一部分的作用。结论是，生长抑素和血清素都未得到充分研究以确定哪一种是所提出的介质。第3章。回顾了所使用的材料和方法。使用了狗，并测量了各种参数——通过滴定法测量胃酸分泌，以血红蛋白为底物通过酶促过程测量胃蛋白酶分泌，通过记录腔内压力测量胃窦运动，通过中性红清除率测量黏膜血流量，通过放射免疫测定法测量生长抑素。（摘要截选至400字）
