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L Limlomwongse

Publications and source records attributed to L Limlomwongse.

33 records · Page 2Linked to original sources
PubMed1983

The acute hypocalcaemic effect of ethanol and its mechanism of action in the rat.

The hypocalcaemic action of ethanol (3 g/kg body weight) was investigated in intact, thyroparathyroidectomized and antrectomized rats. It was found that ethanol administered either intraperitoneally or orally reduced plasma calcium concentrations within 30 min and that this response lasted for 8 h. Additional studies performed in antrectomized and thyroparathyroidectomized rats indicated that neither gastrin nor the hormones parathormone and calcitonin had any effect on the hypocalcaemic effect of ethanol. Investigation of the mechanism of action of ethanol-induced hypocalcaemia involved measurements of calcium efflux from and influx into the plasma pool. Ethanol did not have any effect on the disappearance from plasma of 45Ca administered intravenously at 0 min. In contrast, ethanol was found to enhance the disappearance of 45Ca administered intraperitoneally 17 h prior to the experiment. The interpretation of 45Ca studies was discussed and it was concluded that ethanol-induced hypocalcaemia resulted from a decrease in calcium influx into the plasma. Additional in vitro studies did not indicate the suppressive action of ethanol on the release of calcium from tibias. In conclusion, our results show that the mechanism of hypocalcaemia caused by ethanol is the suppression of calcium release from some tissue(s) into the plasma.

Animals↗
PubMed1983

Calcium metabolism in relation to chronic ethanol ingestion and estrogen deficiency in rat.

The plasma calcium concentration, urinary calcium excretion, total bone calcium content and the rate of calcium uptake and release by tibias were measured in 6 groups of rats which were kept under various treatment protocols for 8 wk. Ovariectomy led to significant hypocalcemia and a decrease in bone calcium content; the former being reversed towards normal by estrogen treatment. Chronic ethanol ingestion reduced the bone calcium content without apparent effect on plasma calcium in intact rat and further reduced (P less than 0.05) the bone calcium content in ovariectomized rats. The calcium uptake by the bone measured by 45Ca injected ip at zero hour was the same among the 6 groups. When 45Ca was injected ip 17 hours earlier, the disappearance of plasma 45Ca was found to be slower in ovariectomized and alcohol treated groups, indicating a higher rate of calcium movement from bone to plasma. Moreover, there was also an increase in the rate of calcium release by tibias after ovariectomy and chronic alcohol ingestion; the release was slightly greater in the condition of ovariectomy plus alcohol. The present investigation thus, provides evidence that ethanol is likely to have a direct stimulatory effect on bone resorption as well as an indirect effect through disrupting ovarian function during chronic administration.

Animals↗
PubMed1983

Effect of estradiol treatment on the secretion and structure of gastric H+ and pepsin-secreting cells in the rat.

Gastrin-stimulated secretory rate of gastric H+ and pepsin were markedly inhibited (P less than 0.001) in ovariectomized rat after 7 days of estradiol treatment (80 micrograms/kg/day) in comparison to ovariectomized untreated rat and sham control. In correlation to the secretions, the majority of parietal cells failed to show the typical ultrastructural transformation associated with active secretion. Pyknotic nuclei with dilatation of nuclear envelope and degenerative changes were observed in the parietal cells. Meanwhile, the chief cell showed inactive characteristics in that a large number of pepsinogen granules were retained in the cells. In contrast, in ovariectomized untreated rat, the rate of gastrin-stimulated H+ and pepsin secretion were not significantly different from the sham (P greater than 0.05). Consistent with secretion, after gastrin stimulation, the morphology and ultrastructure of the parietal cell and chief cell showed active secretory features in a pattern similar to changes observed in sham. The results suggest that impairment in the structure of the functional parts of secretory cells by estrogen treatment was a factor contributing to the inhibition of the gastric secretions.

Animals↗
PubMed1982

Inhibition of gastric H+ secretion, K+-ATPase and K+-phosphatase by estradiol in vivo and in vitro.

The effect of estrogen on the gastric acid secretion and H+-transporting enzymes, K+-ATPase and K+-phosphatase, were investigated in the rat. The maximum H+ secretory rate in response to 1 mM histamine was significantly reduced (P less than 0.05) in both the isolated gastric mucosa obtained from the rats treated with estradiol in vivo for 7 days and the mucosa directly incubated in vitro with estradiol. The inhibitory effect on the gastric enzyme activities in vitro showed a dose-dependent pattern of a noncompetitive type. The result suggested that estradiol may have a direct action on the gastric H+ secretion by inhibiting the H+ transport enzyme activities.

Adenosine Triphosphatases↗
PubMed1981

Possible role and mode of action of gastrin on calcium homeostasis in the rat.

The hypocalcemic effect of gastrin and its possible mode of action were studied in rats. Gastrin (13 micrograms/100 g rat), injected intravenously led to a significant reduction in the plasma calcium concentrations. The release of endogenous gastrin by an intragastric phenylalanine instillation similarly led to a significant hypocalcemia in intact rat but not in antrectomized rat. Moreover, the protective role of endogenous gastrin against hypercalcemia induced by an intraduodenal infusion of CaCl2 (10 mg/100 g rat) was demonstrated. Gastrin (50 microgram/100 g rat) seems to have no influence on the net intestinal absorption of 45Ca. The removal of 45Ca from plasma was also unaffected by gastrin administration. The disappearance rate from plasma of 45Ca administered 17 hr previously was compared in sham, thyroidectomized (TX) and parathyroid-autotransplanted rats receiving saline or gastrin. The faster rate of disappearance of plasma 45Ca from plasma in gastrin-treated TX autoparathyroid-transplanted rats indicated the suppressive action of gastrin on the release of 45Ca from as yet unknown source(s).

Animals↗
PubMed1981

The mechanism of action and target organ of gastrin-induced hypocalcemia.

The hypocalcemia effect of gastrin and the possible role of the hormone in calcium homeostasis have been demonstrated in our previous study. The mechanism involves neither the gastrointestinal absorption nor the removal of calcium from plasma but is possibly due to the suppression of the calcium influx into blood. In searching for the organ(s) involved in the action of gastrin, the following were tested and not found to be directly responsible: stomach, intestine, pancreas, liver, spleen, adrenal gland, kidney, lung, muscle, and red blood cell. After 17 hr of 45Ca administration, the turnover of 45Ca in the tibia was measured. Gastrin was found to suppress the release of 45Ca by 25% within 1 hr. The suppressive effect of gastrin on 45Ca release was also demonstrated in an in vitro preparation which showed that the 45Ca released from prelabeled tibia into the incubating medium was also reduced by gastrin. It was thus concluded that the gastrin-induced hypocalcemia in rat was the result of a suppression of the release of calcium from bone.

Animals↗
PubMed1979

Effect of capsaicin on gastric acid secretion and mucosal blood flow in the rat.

The effect of capsaicin, a pungent ingredient in capsicum fruit, upon gastric acid secretion and mucosal blood flow was assessed in the anesthetized rat. At each 15 minute interval, 0.3 ml saline solution, with or without various doses of pure synthetic capsaicin (the doses varied from 50 to 2,000 microgram/kg rat) was delivered into the gastric lumen via a gastric fistula. The gastric contents were withdrawn after 15 minutes for acid assay and replaced with a new saline solution. Capsaicin of increasing doses (up to 1,000 microgram/kg) progressively increased the acid output. Gastric inhibitors hexamethonium and atropine, completely abolished the acid secretion induced by capsaicin whereas secretin only partially reduced such a response. The systemic blood pressure was not affected by the capsaicin or the method employed. However, the aminopyrine clearance which was the indicator of the gastric mucosal blood flow increased in accordance with the increase in the acid output. It is suggested that the effect of capsaicin on the acid secretion and mucosal blood flow is by the release of endogenous gastric secretagogues which increase both tissue perfusion and the secretory activity.

Aminopyrine↗
PubMed1976

Mechanism of inhibition of gastric acid secretion by hypertonic solutions and vasopressin.

An experiment was performed in female rats in order to assess the influence and mechanism underlying the effects of hyperglycemia, hypertonic saline and vasopressin upon the gastric acid secretion and mucosal blood flow (MBF). Infusion of isotonic saline did not alter acid output and gastric clearance of plasma aminopyrine whereas hypertonic solutions (20% glucose or 3% NaCl) significantly increased plasma osmolality and decreased the acid secretion within 30 min and recovered to normal levels after 2 h. Vasopressin also effectively inhibited acid secretion. Both hypertonic solutions and vasopressin decreased the mucosal blood flow. However, the ratio (R) of MBF to gastric secretory rate which is a helpful guide to the mechanism of secretory inhibition did not significantly change in either case. We concluded that all three agents probably had a direct action on secretion rather than decreasing MBF. The mechanism of inhabition of acid secretion and its relationship to MBF was suggested and discussed.

Animals↗
PubMed1969

Ion transport and the development of hydrogen ion secretion in the stomach of the metamorphosing bullfrog tadpole.

Isolated bullfrog tadpole stomachs secrete H(+) by stage XXIV of metamorphosis, when tail reabsorption is nearly complete. At this stage the PD shows characteristic responses identical to those of the adult. The appearance of HCl secretion correlates well with other studies showing the morphogenesis of oxyntic cells. Prior to the development of H(+) secretion tadpole stomachs maintain a PD similar in polarity and magnitude to that of the adult; i.e., secretory (S) side negative with respect to the nutrient (N) side. The interdependence with aerobic metabolism appeared to increase progressively through metamorphosis; however, glycolytic inhibitors always abolished the PD. Isotopic flux analysis showed that the transepithelial movement of Na(+) was consistent with passive diffusion, whereas an active transport of Cl(-) from N to S was clearly indicated. Variations in [Na(+)], [K(+)], and [Cl(-)] in the bathing solutions induced changes consistent with the following functional description of the pre-H(+)-secreting tadpole stomach. (a) The S side is relatively permeable to Cl(-), but not to Na(+) or K(+). (b) An equilibrium potential for K(+) and Cl(-) exists at the N interface. (c) Ouabain abolishes the selective K(+) permeablity at the N interface and reduces the total PD. (d) Effects of Na(+) replacement by choline in the N solution become manifest only below 10-20 mM. It is concluded that prior to development of H(+) secretion, the tadpole gastric PD is generated by a Cl(-) pump from N to S and a Na(+) pump operating from the cell interior toward the N side.

Animals↗