Mobilization and formation of histamine in the gastric mucosa as related to acid secretion
Mobilization and formation of histamine in the gastric mucosa as related to acid secretion
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胃粘膜中组胺的动员和形成与胃酸分泌有关
DOI：
10.1113/jphysiol.1964.sp007494
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发表时间：
1964
期刊：
影响因子：
--
通讯作者：
R. Thunberg
中科院分区：
文献类型：
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作者：
G. Kahlson;E. Rosengren;D. Svahn;R. Thunberg
目前的工作起源于两个独立的研究。首先，决定研究大鼠的酸分泌，其中通过抑制双司他胺的形成使大鼠胃粘膜的组胺含量显著降低。众所周知，在喂食吡哆醇缺乏饲料的大鼠中注射氨基脲会极大地降低组胺的形成速率和含量，使其在各种组织中的含量降至正常水平的一小部分，特别是在胃粘膜中（Kahlson & Rosengren，1959; Kahlson，Rosengren & Thunberg，1963）。在这种抑制下，发现胃粘膜响应于胃泌素注射而正常分泌。因此，在本研究的早期阶段，似乎不确定粘膜中存在的组胺是否是激发酸分泌所必需的。同时进行了实验，以研究Hunt（1957）注意到的再喂养大鼠某些胃粘膜细胞有丝分裂指数增加的现象是否伴随着组氨酸脱羧酶水平的相应增加。由于在各种组织中发现了细胞更新与组氨酸脱羧酶活性（组胺形成能力，HFC）水平之间的相关性（参考文献见Kahlson，Rosengren和Steinhardt，1963），因此认为该研究是有意义的。在这项研究的过程中，人们发现，再喂养以及注射纯化的胃泌素引起的壁细胞携带粘膜（体）的HFC升高到禁食水平的许多倍。即使是一小部分的组氨酸脱羧酶活性持续抑制组胺形成后，被发现是类似的喂养或胃泌素升高。有了后一发现，决定将研究主要限于粘膜HFC在刺激酸分泌中所起作用的实验。其中一些观察结果的初步报告已提交给生理学会（Kahlson，Rosengren，Svahn和Thunberg，1963）。
The present work originated in two independent studies. First, it was decided to investigate the acid secretion in rats in which the histamine content of the gastric mucosa had been strongly reduced by subjecting the animals to inhibition of bistamine formation. It was known that semicarbazide injected in rats fed on a pyridoxine-deficient diet would very greatly diminish both the rate of formation and the content of histamine to a small fraction of normal in various tissues, particularly in the gastric mucosa (Kahlson & Rosengren, 1959; Kahlson, Rosengren & Thunberg, 1963). Under such inhibition it was found that the gastric mucosa secreted normally in response to injections of gastrin. At an early stage of the present work it thus appeared uncertain whether the histamine present in the mucosa was essential for the excitation of acid secretion. Concurrently experiments were done to investigate whether the phenomenon of increased mitotic index of certain gastric mucosal cells of rats on re-feeding, which was noted by Hunt (1957), would be accompanied by a corresponding increase in the level of histidine decarboxylase. This search was considered of interest since a correlation between cell renewal and level of histidine decarboxylase activity (Histamine-Forming Capacity, HFC), had been found in various tissues (for references see Kahlson, Rosengren & Steinhardt, 1963). In the course of this investigation it was found that re-feeding as well as injection of purified gastrin evoked an elevation of HFC of the parietal cell-carrying mucosa (corpus) to many times the fasting level. Even the small fraction of histidine decarboxylase activity persisting after inhibition of histamine formation was found to be similarly elevated by feeding or gastrin. With this latter discovery it was decided to confine the study mainly to experiments on the part played by mucosal HFC in inciting acid secretion. A preliminary communication of some of these observations has been given to the Physiological Society (Kahlson, Rosengren, Svahn & Thunberg, 1963).