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Biomedical subjects

J Kumagai

Publications and source records attributed to J Kumagai.

At least 19 recordsLinked to original sources
PubMed1990

[The effect of modified sham-feeding on gastrin-stimulated gastric secretion in patient with duodenal ulcer].

Patients with duodenal ulcer were classified into responders to H2-receptor antagonist and non-responders in whom duodenal ulcer did not heal within three months with the antagonist. In these patients and healthy controls, modified sham-feeding (MSF) test was performed to elucidate the pathophysiological differences between these groups, especially vagal activity of acid output. After tetragastrin 4 micrograms/kg/hr infusion for one hour, MSF was superimposed to the infusion (G + MSF). The acid output of non-responders (8 cases) and controls (8 cases) significantly increased in G + MSF. On the other hand, the acid output of responders (6 cases) significantly decreased. The acid output of non-responders in G + MSF was also significantly higher than that of controls. The results suggest that vagal activity of non-responders is higher than responders, and that there is disturbance of inhibitory mechanism in vagal system.

Adult↗
PubMed1989

Characteristics of spermidine uptake by isolated rat enterocytes.

Eukaryotic cells require polyamines for growth. The supply of polyamines to growing cells may be increased either by new synthesis or increased uptake. We have recently shown that putrescine uptake by isolated rat enterocytes is energy dependent, saturable, and ouabain insensitive. Although putrescine uptake was inhibited by putrescine and cadaverine, it was not inhibited by equal concentrations of spermine and spermidine. These data indicated that a carrier mechanism separate from that putrescine existed for spermidine and spermine. In the current study spermidine uptake by isolated enterocytes was saturable, temperature dependent, and inhibited by 1 mM KCN. Kinetic analysis resulted in a Km = 2.51 x 10(-6) M and a Vmax = 3.57 x 10(-12) mol.10(6) cells-1.15 min-1. Spermidine uptake was 70% inhibited by 1 mM ouabain. Replacement of sodium by choline, lithium, tetramethylammonium, or N-methyl-D-glucamine also inhibited spermidine uptake. Replacement of Na+ by mannitol or sucrose, however, depressed uptake but not significantly. Spermidine uptake was inhibited by 1 mM ouabain. Spermidine uptake was inhibited by relatively low concentrations of spermine and high concentrations of putrescine; while putrescine uptake was inhibited by relatively high concentrations of both spermine and spermidine. Kinetic data indicated that spermidine and spermine share a carrier that is distinct from the one mediating the uptake of putrescine. While spermidine uptake does not appear to depend on Na+ cotransport, it may be dependent on the electrical gradient established by the Na+-K+-ATPase.

Amino Acids↗
PubMed1988

Characteristics of putrescine uptake in isolated rat enterocytes.

Polyamines are necessary for the growth of eukaryotic cells and are supplied either by new synthesis or cellular uptake. To our knowledge, no information is available on polyamine uptake by gastrointestinal cells. In the current study, isolated villous enterocytes from the rat accumulated putrescine to an eightfold concentration gradient. Uptake was temperature dependent, saturable, and inhibited by 1 mM KCN. Kinetic analysis showed a Km of 1.23 X 10(-5) M and a Vmax of 2.60 X 10(-10) mol.10(6) cells-1.15 min-1. Enterocytes from the distal one-fourth of the gut showed the highest rate of uptake. Putrescine uptake was inhibited by cadaverine and spermine but not by the amino acids asparagine, AIB, or leucine. Sodium replacement by choline, lithium, N-methyl-D-glucamine, or tetramethylammonium significantly inhibited uptake, but replacement of Na+ by sucrose or mannitol was without effect. The inhibition observed was believed to be due to the ability of the cations to interact in some way with the carrier. Neither ouabain nor digitoxigenin had any effect on uptake. These data indicate that putrescine is accumulated by villous enterocytes by a carrier-mediated process that does not appear to involve Na+ contransport.

Animals↗
PubMed1986

The role of carbonic anhydrase in gastric mucosal protection with special reference to H+ back diffusion and concomitant metabolic acidosis induced by acetazolamide.

It is suggested that carbonic anhydrase is implicated not only in gastric acid secretion, but in mucosal protection. It was reported that acetazolamide induced gastric mucosal lesions. But acetazolamide also caused concomitant metabolic acidosis by inhibiting H+ secretion from renal tubules. We investigated whether concomitant metabolic acidosis is implicated in gastric mucosal lesions induced by acetazolamide in vivo. We also evaluated the effect of acetazolamide on gastric H+ back diffusion in vivo. Correction of metabolic acidosis with sodium bicarbonate had no effect on the degree of the gastric mucosal lesions. Acetazolamide caused no change in gastric H+ and Na+ flux. These results suggest that metabolic acidosis induced by acetazolamide is not implicated in gastric mucosal lesions. Carbonic anhydrase has no effect on H+ back diffusion but may be implicated in mucosal protection by the disposition of back diffused H+ into the gastric mucosa.

Acetazolamide↗
PubMed1986

Cyclic AMP in gastric juice does not reflect histamine H2 receptor activity in Heidenhain pouch dog.

It is strongly believed that cAMP mediates histamine H2 receptor activity, but does not mediate gastrin and acetylcholine stimulation of gastric acid secretion. Therefore, cAMP production could be a marker of H2 receptor activity. Whether endogenous histamine mediates gastrin and/or acetylcholine stimulation, at least partially, remains to be elucidated. If cAMP in the gastric juice reflects H2 receptor activity, we can investigate whether endogenous histamine mediates gastrin and/or acetylcholine stimulation in vivo. In this study, we investigated whether cAMP in the gastric juice reflected histamine H2 receptor activity in the Heidenhain pouch dog in vivo using different kinds of inhibitors of gastric secretion. Our hypothesis was as follows: Upon betazole stimulation, cimetidine, an H2 receptor antagonist, should decrease cAMP output into the gastric juice, but omeprazole, an H+, K+-ATPase blocker, should not, because it blocks at a site more peripheral than the H2 receptor and the production of cAMP. Sixty minutes after betazole administration, 4.0 mumol/kg of cimetidine and 0.18 mumol/kg omeprazole were administered intravenously and they inhibited gastric juice volume to a similar degree, that is, 49.6% and 52.1%, respectively. However, omeprazole caused a greater decrease in cAMP output than cimetidine. Inhibition with 4 mumol/kg/h of cimetidine or 0.2 mumol/kg of omeprazole from the beginning of betazole stimulation also caused similar decreases in gastric juice volume, 66.6% and 60.6%, respectively. Both inhibitors decreased cAMP output into the gastric juice in a similar fashion in the first two 30 minute periods. These results do not agree with our hypothesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗