Effect of acid blockade on gastric histamine in mice

Vagotomy and omeprazole effectively inhibited 2-deoxy-d-glucose (–91%) and pentagastrin (–72%) stimulated acid production in mice, respectively. Both vagotomy and omeprazole treatment were accompanied by massive increases in histamine secretion (8-fold or more, during both basal and stimulated states). Mucosal stores of histamine, however, were not depleted. Similar rises in luminal histamine have been observed in patients treated in these ways. The mouse model may thus be suitable to elucidate the kinetics of histamine release in patients.     

Effect of adrenalectomy on gastric secretion induced by food or histamine in dogs

The effect of total adrenalectomy on gastric function was studied in chronic experiments on dogs with Pavlov gastric pouches and Basov fistulas. The decrease in the level of maximal secretion of juice was connected with changes in the hemodynamics of the stomach. A tendency for the level of acid formation in the stomach to decrease was observed. Significant differences were found in the character of secretion of proteolytic enzymes in response to different types of activators of secretion, indicating the specific nature of activation of the gastric secretory system in the case of each stimulus, as well as differences in the effect of adrenalectomy on secretion induced by them.Department of Human and Animal Physiology and Laboratory of Physiology, Research Institute of Biology and Biophysics, Tomsk University. (Presented by Academician of the Academy of Medical Sciences of the USSR D. D. Yablokov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 85, No. 5, pp. 531–533, May, 1978.     

Gastrointestinal histamine after gastric irradiation in the mouse

A single dose of 9 or 15 Gy of X-rays was given to the stomach of mice. Gastric histamine formation capacity (HFC) rose in a dose-related fashion during days 4 to 11 after irradiation. This rise coincided with a dose-dependent fall in gastric mural histamine concentration. 15 Gy X-rays also resulted in a transient loss of body weight (days 4–8 after irradiation). These results suggest that irradiation of the stomach mobilizes gastric histamine and that gastric histamine stores may be radiosensitive.     

Inhibition of histamine biosynthesis and gastric function in the rat: effect on pentagastrin-induced gastric acid secretion

A very simple and rapid method to measure gastric acid secretion in the conscious unoperated fasted rat is reported. Antisecretory activity of cimetidine and hypersecretory activity of pentagastrin are detected by this procedure. Pentagastrin induces gastric acid secretion and causes an increase by 2-fold in histidine decarboxylase activity. There is a delay between the increase of gastric acid output and the appearance of histidine decarboxylase activity. Co-administration of monofluoromethyl histidine, a specific irreversible inhibitor of histidine decarboxylase, does not modify the peak response to pentagastrin but shortens the duration of stimulation. We suggest from this data that histamine biosynthesis is needed for maintenance of elevated gastric acid secretion.     

Effect of thyroxine on histamine metabolism in mice

Mice were injected with saline or thyroxine 10 μg, for periods of 1 or 4 days, given inhibitors of histamine catabolism, injected with¹⁴C-L-histidine, and killed 10 minutes later. Assay of tissues for¹⁴C-histamine showed no meaningful differences between the two groups. The hyperthyroid condition of the test group was shown by a variety of criteria. Under similar conditions no effect on catabolism of injected¹⁴C-histamine was observed. However, after treatment of mice for 8 days with saline or thyroxine, and then injection of¹⁴C-L-histidine (inhibitors of histamine catabolism were omitted) there was an increase of¹⁴C-histamine in kidney and urine to 5 and 7 times that of controls. Assay of kidney for histamine methylation in vitro after 1 or 8 days of thyroxine treatment showed no significant effect in the former but a marked reduction of activity in the latter; in the 8 day group kidney histidine decarboxylase activity was increased to nearly 70 times that of control. A time study of thyroxine effects showed that histidine decarboxylase activity was normal after 1 day, definitely elevated after 2 days and very high after 4 days. None of our data suggested that altered histamine metabolism could be involved in production of the hyperthyroid state. However, from the marked changes observed as early as day 2, it could be concluded that the highly active histidine decarboxylase is mainly localized in a region of kidney from which most newly-formed histamine is directly excreted in urine without entering the systemic circulation; if so, mice are the fourth species in which evidence for this phenomenon has been observed.     

The release of histamine during gastric acid secretion in conscious rats

1. Conscious gastric-cannulated rats were given [(3)H]histidine and aminoguanidine by dosage procedures intended to build up fast-turnover and slow-turnover pools of tissue [(3)H]histamine. Acid secretion was stimulated by I.V. infusion of pentagastrin, and the [(3)H]histamine content of gastric juice and excretion in urine were determined at 30 min intervals.2. The amount of [(3)H]histamine in gastric juice derived from either a slow-turnover or fast-turnover pool was very low in unstimulated animals, and was not altered during pentagastrin-stimulated acid secretion.3. From a slow-turnover pool pentagastrin caused increased urinary excretion of [(3)H]histamine. This was abolished by gastrectomy, so that the [(3)H]histamine liberated by pentagastrin from this pool appears to have been derived from the stomach. Evidence was not found for the existence of a slow-turnover histamine pool in the glandular mucosa of the stomach, and the source within the stomach of this pentagastrin-liberated histamine is thus uncertain.4. From a fast-turnover pool pentagastrin did not cause an increased urinary excretion of [(3)H]histamine. The amount of [(3)H]histamine excreted by gastrectomized rats was not different from that produced by gastric-cannulated animals. This suggests that a high proportion of urinary histamine derived from a fast-turnover pool was non-gastric in origin.5. Differences in the time scale of [(3)H]histamine release and acid secretion were not found. In some experiments the urinary output of [(3)H]histamine was prolonged beyond the end of pentagastrin administration and gastric acid secretion. However, the overall data do not suggest that urinary histamine output and gastric acid secretion take different time courses.     

Effect of histamine and NαNα-dimethylhistamine on gastric acid secretion and mucosal blood flow in Heidenhain-pouch dogs

Conclusions It is concluded that in accordance with numerous previous reports acid secretion in response to histamine is mediated by H₂-receptors. The powerful effect of histamine on GMBF is at least in part mediated by H₁-receptors. Since NDMH is much less effective than histamine in increasing GMBF and is not inhibited by mepyramine, this compound is more selective in stimulating histamine H₂-receptors than histamine.