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Biomedical subjects

M Kondoh

Publications and source records attributed to M Kondoh.

82 records · Page 5Linked to original sources
PubMed1988

[Early esophageal cancer discovered 6 months after endoscopic injection sclerotherapy of esophageal varices].

Early esophageal cancer was discovered in a 55-year-old male with liver cirrhosis six months after the start of treatment for esophageal varices by a series of endoscopic sclerotherapeutic injections using 5% ethanolamine oleate. A histological examination of the entire length of the resected esophageal wall revealed a carcinomatous lesion oralwards and far removed from the lesion where subsequent changes due to sclerotherapy were prominent. Further, the causal relationship between sclerotherapy and carcinoma is discussed.

Carcinoma, Squamous Cell↗
PubMed1987

Influence of neural blockages and proglumide on rat pancreatic enzyme secretion in response to intraluminal fatty acid.

Effects of neural blockages on pancreatic enzyme secretion in response to infusing fatty acid into the lumen were investigated using anesthetized rats, equipped with bile-pancreatic and duodenal cannulae, to evaluate the relative contribution of the neural and the hormonal mediations in the pancreatic response. Oleate (0.2 ml) was injected as a bolus into the rat duodenum, and the trypsin output in bile-pancreatic juice was monitored to determine the pancreatic enzyme secretion response with continuous return of bile-pancreatic juice to the intestine. When anticholinergic agents such as atropine sulfate and scopolamine were administrated, although basal level in pancreatic enzyme secretion fell, the increase of pancreatic enzyme secretion from basal level after stimulation by oleate was not significantly different from that of the control (no blockage). However, the ganglion blocker, hexamethonium, inhibited the pancreatic enzyme secretion in response to oleate by 94%. An adrenergic blocker, guanethidine, also led to as much of a decrease as the ganglion blocker-induced decrease. Adrenergic alpha- and beta-blockers partially, but not completely, inhibited the enzyme secretion. Adrenergic blockage also suppressed the basal level in pancreatic enzyme secretion. On the other hand, a specific CCK antagonist, proglumide, significantly inhibited pancreatic enzyme secretion induced by oleate in the presence of scopolamine. These observations suggest that pancreatic enzyme secretion in response to oleate is primarily mediated by CCK and that adrenergic modulation may play an important role in the CCK-mediated pancreatic enzyme secretion in response to oleate, although interpretation of these results may have some restriction related to anesthesia.

Adrenergic alpha-Antagonists↗
PubMed1985

Changes in the intraluminal protein digestion of pancreatic duct-ligated rats.

After ligature of the pancreatic duct (PDL), the body weight of rats decreased for several days, but began to increase from day 7, returning to that at the time of the operation on day 14. In these PDL animals, the weight gain was not due to improved digestion resulting from duodenal leakage of pancreatic enzymes or a compensatory increase of proteolytic enzyme activities in the intestinal mucosa. There was no significant difference in pepsin activities in the gastric contents and mucosa of control and PDL rats. However, acidic proteolytic activity, with a pH range between 1 and 4 and an optimum at pH 2.8, was found to be extremely high in the intestinal contents of PDL rats. Furthermore, the intraluminal pH of PDL rats was maintained below 4.0, especially in the upper small intestine, because of the absence of pancreatic bicarbonate secretion, suggesting that compensatory digestion by acidic proteolysis accounted in part for the growth of PDL rats. The transit time of orally administered material through the gastrointestinal (GI) tract in PDL rats was longer than that in control rats on days 7 and 14. These results suggest that the weight gain of PDL rats was caused by compensatory digestion by acidic proteolysis in the small intestine and prolongation of the transit time through the GI tract.

Animals↗
PubMed1984

Effect of sodium saccharin on rat pancreatic enzyme secretion.

Intragastric administration of casein, oleic acid, or polyvinylpyrrolidone resulted in a marked increase in the pancreatic secretion of enzymes, and the administration of 0.03% sodium saccharin, at the concentration permitted in soft drinks, inhibited this increase with these substances. The stimulation of secretion of pancreatic juice-bile mixture by these substances was also inhibited by administration of sodium saccharin. Intravenous injection of CCK-PZ (cholecystokinin-pancreozymin) during inhibition by sodium saccharin, caused a rapid increase in amylase output, suggesting that sodium saccharin acts on the site(s) of CCK-PZ release to prevent its secretion even in the presence of a stimulant, but does not reduce the sensitivity of the pancreas to CCK-PZ. Sodium saccharin seemed to have an effect on secretin release similar to that on CCK-PZ release, judging from the results for the volume of juice-bile mixture.

Amylases↗
PubMedDate not supplied

Prevention of the febrile reaction occurring on reinfusion of cell-free and concentrated autogenous ascites.

The febrile reaction that occurs on reinfusion of ascites was studied. Intravenous reinfusion of ascites was performed 213 times in 63 cases of ascites, which were refractory to treatment with various drugs including diuretics. In order to prevent fever on reinfusion of ascites, a screen filter and a depth filter were used; the results were more favorable with the screen filter. Fibrin was considered to be one of the substances removable by the screen filter. HPLC analysis of the filtered and concentrated ascites, after passage through the screen filter, revealed a fraction corresponding to albumin. Intravenous injection of this fraction into rabbits caused fever. Although the screen filter cannot completely prevent fever on reinfusion of ascites, it appears useful to prevent fever in some patients.

Adult↗