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Biomedical subjects

M Fujimura

Publications and source records attributed to M Fujimura.

At least 163 records · Page 9Linked to original sources
PubMed1985

Inhibitory effect of N-(3', 4'-dimethoxycinnamoyl) anthranilic acid (N-5') on SRS-A mediated bronchoconstriction in the guinea pig in vivo.

Slow-reacting substance of anaphylaxis (SRS-A) is an important factor mediating bronchoconstriction in asthma. We developed a guinea pig model for SRS-A-mediated bronchoconstriction induced by antigen inhalation. Using this model, we investigated the effect of N-(3', 4'-dimethoxycinnamoyl) anthranilic acid (N-5'), a new anti-allergic drug, on the bronchoconstriction. FPL 55712 inhibited most of the bronchoconstriction induced by antigen inhalation. N-5' inhibited the antigen-induced bronchoconstriction in a dose-dependent fashion. Intraperitoneal administration of 200 mg/kg N-5' was effective for 40 min after antigen inhalation, while the effect of 60 mg/kg lasted only 7 min. On the other hand, 200 mg/kg N-5' showed no inhibitory effect on the bronchoconstriction caused by direct inhalation of leukotriene C4, a component of SRS-A. These findings indicate that one of the anti-allergic actions of N-5' is due to inhibition of synthesis and/or release of SRS-A.

Animals↗
PubMed1985

Comparison of hepatic elimination of different forms of cholecystokinin in dogs. Bioassay and radioimmunoassay comparisons of cholecystokinin-8-sulfate and -33-sulfate.

The influence of hepatic transit on the ability of exogenous cholecystokinin-8-sulfate and -33-sulfate (CCK-8 and CCK-33, respectively) to stimulate gallbladder contraction and exocrine pancreatic secretion, as well as on the peripheral plasma concentration of each agent, was evaluated in five conscious dogs with pancreatic and gallbladder fistulas and complete portacaval transposition. The gallbladder pressure increments after portal administration of CCK-8 (0.125, 0.25, 0.50, and 1.0 microgram/kg per h for 5 min) were diminished by 36, 45, 39 and 25%, respectively, in comparison with those obtained with systemic administration of identical doses of CCK-8 (P less than 0.05). In a subsequent experiment, the integrated pancreatic juice volume, bicarbonate, and protein secretion were diminished by 22, 32, and 48%, respectively, during a 30-min infusion of CCK-8 (0.10 micrograms/kg per h) into the portal venous system, in comparison with the results obtained with systemic administration of CCK-8 (P less than 0.05). In contrast, the gallbladder pressure and pancreatic exocrine secretory responses to portal administration of CCK-33 did not differ significantly (P greater than 0.05) from the results obtained with systemic administration of CCK-33. Radioimmunoassay for CCK-8 in plasma showed that the integrated CCK-8 value during portal administration was significantly lower (P less than 0.05) than it was during systemic administration. The results for CCK-33, however, did not vary, whether it was given by a systemic or portal route (P greater than 0.05). Thus, the present study demonstrates that CCK-8 is partially inactivated by the liver whereas CCK-33 is not, which suggests that CCK-3 in the circulation may play a significant role in the physiologic regulation of the gallbladder and exocrine pancreas.

Animals↗
PubMed1985

Lymphoid interstitial pneumonia: findings at bronchoalveolar lavage.

In a patient with lymphoid interstitial pneumonia (LIP), confirmed by open lung biopsy, immunological derangement was evaluated using bronchoalveolar lavage fluid and peripheral blood. In the bronchoalveolar lavage fluid there were 20% null cells, 0% B cells, 77% alveolar macrophages and 3% T cells; in the peripheral blood these were 12% null cells, 43% B cells, 26% mononuclear phagocyte system cells, 2% double marker cells and 17% T cells. Thus there was T cell depletion and null cell increment in bronchoalveolar lavage, in contrast to T cell depletion and increment of B cells and mononuclear phagocyte system cells in the peripheral blood.

Adult↗
PubMed1985

Importance of the ileum in neurotensin released by fat.

Neurotensin is a potent stimulant of pancreatic exocrine secretion. Ileal mucosa is the storage site for about 90% of total neurotensin. Release occurs rapidly after a fatty meal and during perfusion of the duodenum and jejunum with fat but not during perfusion of the ileum with fat. To determine the origin of neurotensin released after fat stimulation, we studied the pattern of release of neurotensin before and after resection of the distal two thirds of the small bowel. Six dogs with gastric and duodenal fistulas were studied on different days. All dogs received infusions (in random order) of intraduodenal corn oil (Lipomul) (3 ml/kg/hr) and intravenous calcium chloride (0.36 mmol/kg intravenous bolus, followed by 0.36 mmol/kg/hr infusion) before and 6 weeks after resection of the distal two thirds of the small bowel with preservation of the ileocecal valve. Plasma levels of neurotensin were measured by specific radioimmunoassay. We found that release of neurotensin, in response to both intraduodenal Lipomul and intravenous calcium chloride stimulation, was abolished by resection of the distal small bowel. Before surgery, Lipomul-stimulated release of neurotensin rose to a peak concentration of 51 +/- 17 pg/ml at 30 minutes. After surgery there was no release (the levels were unchanged from basal). Before surgery, intravenous calcium chloride produced a peak release of neurotensin (52 +/- 15 pg/ml) 2 minutes after bolus injection. After surgery, neurotensin was not released by intravenous calcium. We conclude that the source of neurotensin released by perfusion of the proximal gut and by intravenous calcium infusion is the ileum. The release of neurotensin from the distal gut appears to be dependent on a signal from proximal to distal gut. The identity of the signal is unknown but is either a nerve reflex or a peptide agent.

Animals↗
PubMed1985

Effect of a Ca2+ antagonist, nifedipine, on the experimental asthma mediated mainly by slow reacting substance of anaphylaxis.

In the asthmatic model mainly mediated by the endogenous slow reacting substance of anaphylaxis (SRS-A) induced by the antigen inhalation to passively sensitized guinea pigs, continuous intravenous infusion of nifedipine (Adalat) at a speed of 7 micrograms/kg/min depressed the airway open pressure by about 68% compared to the saline-treated group and produced a delay in the time to peak response. Moreover, nifedipine inhibited the response of the peripheral airway more strongly than that of the central airway. The same concentration of nifedipine inhibited the airway open pressure by about 43% compared to the saline-treated group in the asthmatic model induced by the inhalation of leukotriene C4. The effect of nifedipine on the central airway was shorter in duration than that on the peripheral airway. The inhibitory effect of nifedipine on the airway response was greater in the asthmatic model mediated mainly by the endogenous SRS-A induced by the antigen inhalation than in the asthmatic model produced by the inhalation of leukotriene C4.

Airway Resistance↗