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Biomedical subjects

M Fujimura

Publications and source records attributed to M Fujimura.

At least 109 records · Page 6Linked to original sources
PubMed1988

[Hydronephrosis presenting as the first sign of malignant lymphoma of the small intestine: report of a case].

A 45-year-old man was admitted to hospital on November 26, 1985 with the chief complaint of left hypochondrial pain. Excretory and retrograde pyelography revealed left hydronephrosis due to extrinsic obstruction of ureter. Computerized tomography and angiography revealed that a tumor of the small intestine was the cause of ureteral obstruction. In addition to the presence of a tumor, a fistula in the small intestine was disclosed on the upper gastrointestinal series. During the operation, a large mass which involved several organs was identified without mobility. The sophisticated operation was composed of wide resection of small intestine including the tumor, left hemicolectomy, left nephroureterectomy, splenectomy, partial pancreatectomy, duodeno-ileostomy and transverse sigmoidostomy was done on December 19, 1985. Pathological diagnosis was malignant lymphoma, diffuse small cell type infiltrating ureter, kidney and perirenal connective tissue. Because of poor postoperative course systemic chemotherapy was not performed and he died of disseminated intravascular coagulation on April 2, 1986.

Humans↗
PubMed1988

Interaction of neurotensin, secretin and cholecystokinin on pancreatic exocrine secretion in conscious dogs.

The results of previous studies from our laboratory have shown that neurotensin can stimulate pancreatic secretion of bicarbonate and protein. This study was done to compare the stimulatory action of neurotensin on pancreatic exocrine secretion in conscious dogs to those of secretin and cholecystokinin (CCK). Six dogs with chronic pancreatic and gastric fistulas were given hydrochloric acid intraduodenally or CCK-8 intravenously to produce maximal bicarbonate or protein secretion. Neurotensin was then given intravenously in combination with intraduodenal hydrochloric acid or intravenous CCK-8. Incremental bicarbonate outputs in response to intraduodenal hydrochloric acid alone were measured and compared with intraduodenal hydrochloric acid plus intravenous neurotensin. Intravenous administration of neurotensin augmented pancreatic bicarbonate and protein secretory responses to a maximal dose of intraduodenal hydrochloric acid. Incremental protein responses to intravenous CCK-8 alone were measured and compared to intravenous CCK-8 plus intravenous neurotensin. Incremental bicarbonate responses to intravenous CCK-8 alone were compared with intravenous CCK-8 plus intravenous neurotensin. Similarly, intravenous neurotensin augmented pancreatic protein and bicarbonate secretory responses to a maximal dose of intravenous CCK-8. The results of this study indicate that neurotensin may stimulate pancreatic secretion of protein and bicarbonate by mechanisms which are different from those of CCK and secretin. Neurotensin apparently exerts its action through specific neurotensin receptors.

Animals↗
PubMed1987

Peptide YY interacts with secretin and duodenal acidification to inhibit gastric acid secretion.

Previous studies have indicated that plasma levels of peptide YY (PYY) increase significantly after a meal. The purpose of this study was to characterize the interaction of PYY and secretin in the inhibition of gastric acid secretion, and to determine whether PYY can influence acid-induced inhibition of gastric acid secretion in conscious dogs. I.v. administration of PYY at 200 pmol/kg/h inhibited pentagastrin (1 microgram/kg/h)-stimulated gastric acid output (P less than 0.05). PYY further augmented i.v. secretin-induced inhibition of pentagastrin-stimulated gastric acid output by 32 +/- 7%, and intraduodenal hydrochloric acid-induced inhibition of pentagastrin-stimulated gastric acid output by 40 +/- 12%. The mean integrated release of secretin response to duodenal acidification (3.9 +/- 1.0 ng-[0-60] min/ml) was not affected by PYY (3.3 +/- 0.9 ng-[0-60] min/ml). The present study demonstrates that PYY can interact with secretin and duodenal acidification in an additive fashion to inhibit pentagastrin-stimulated gastric acid secretion. Our results suggest that several hormones that are released postprandially can interact with each other to inhibit gastric acid secretion.

Animals↗
PubMed1987

Peptide YY inhibits nutrient-, hormonal-, and vagally-stimulated pancreatic exocrine secretion.

Peptide YY (PYY) is a recently isolated gut peptide that is found primarily in the mucosal endocrine cells of the terminal ileum, colon, and rectum of several mammalian species, including humans. The purpose of this study was to characterize the effect of PYY on pancreatic exocrine secretion in six conscious dogs prepared with pancreatic and gastric fistulas. In control experiments, pancreatic exocrine secretion was stimulated by either intravenous (i.v.) administration of secretin (100 ng/kg/h), cholecystokinin-8 (50 ng/kg/h), neurotensin (5 micrograms/kg/h), or 2-deoxy-D-glucose (75 mg/kg); or by the intraduodenal infusion of hydrochloric acid (4 mEq/h), a mixture of amino acids (phenylalanine + tryptophan at 5 mmol/h), sodium oleate (9 mmol/h), or a liquid meal. On separate days, PYY (12.5, 25, 50, 100, 200, or 400 pmol/kg/h) was given intravenously in combination with one of the above pancreatic secretagogues. Intravenous PYY at 200 and 400 pmol/kg/h inhibited secretin-stimulated pancreatic bicarbonate output significantly (p less than 0.05). Pancreatic bicarbonate and protein responses to all pancreatic secretagogues were reduced significantly (p less than 0.05) by PYY at 400 pmol/kg/h. Intravenous administration of atropine (0.6 mg bolus, followed by 0.02 mg/kg/h) did not abolish the ability of PYY to inhibit secretin-stimulated pancreatic bicarbonate secretion. This study demonstrates that PYY can inhibit nutrient-, hormonal-, and vagally-stimulated pancreatic exocrine secretion in the dog; its mechanism of action appears to be independent of cholinergic innervation.

Amino Acids↗
PubMed1987

Inhibitory action of peptide YY on gastric acid secretion.

The purpose of this study is to investigate the effect of peptide YY (PYY) on pentagastrin-, histamine-, and bethanechol-stimulated gastric acid secretion and the possible mechanisms by which PYY inhibits gastric acid secretion. Six mongrel dogs with chronic gastric and duodenal fistulas were given an intravenous infusion of pentagastrin (0.5 microgram . kg-1 . h-1), histamine (18 micrograms . kg-1 . h-1), or bethanechol (80 micrograms . kg-1 . h-1) either alone or simultaneously with intravenous PYY (100, 200, 400, pmol . kg-1 . h-1). PYY (100, 200, 400 pmol . kg-1 . h-1) inhibited pentagastrin-stimulated gastric acid secretion in a dose-dependent manner. PYY (400 pmol . kg-1 . h-1) did not depress bethanechol-stimulated gastric acid secretion. PYY (400 pmol . kg-1 . h-1) also failed to inhibit histamine-stimulated gastric acid secretion. Furthermore, PYY inhibit pentagastrin-stimulated gastric acid secretion in the face of atropine, vagotomy, or indomethacin treatment. These findings indicate that the inhibitory action of PYY on gastric acid secretion is in part independent of long and short cholinergic pathways. These findings also indicate that the inhibitory mechanism of PYY is independent of prostaglandin synthesis. Our findings are discussed in relation to previous reports regarding the effects of PYY on gastric acid secretion.

Animals↗
PubMed1987

Primary hemangiopericytoma of the heart associated with pseudoaneurysm of the pulmonary artery--a case report.

A thirty-three-year-old male with malignant hemangiopericytoma of the right ventricular outflow tract and the pulmonary artery associated with pseudoaneurysm formation at the latter is presented. Contrast computed tomography was helpful in diagnosing the pseudoaneurysm of the pulmonary artery. The positional change of the murmur, with a tumor plop caused by the pedunculated tumor of the right ventricular outflow tract, was detected.

Adult↗
PubMed1987

[Malignant hemangiopericytoma of the right ventricular outflow tract and the pulmonary artery: a case report].

A case of malignant hemangiopericytoma of the right ventricular outflow tract and the pulmonary artery associated with formation of a pseudoaneurysm in the latter is presented. This 33 year-old man had a four month history of illness. From the surgical point of view, all non-invasive modalities including phonocardiography, M-mode and two-dimensional echocardiography, radionuclide angiocardiography and contrast computed tomography underestimated the extent of the tumor as compared with the selective cineangiographic estimation. Therefore, it was suggested that in some situations where surgery is contemplated, a combination of non-invasive methods and cineangiography is essential to obtain sufficient diagnostic information, although the introduction of catheters into the right-sided cardiac chambers containing a mass might be hazardous because of potentiality dislodging portions of a tumor or adherent thrombus. Concerning pericardial abnormalities, contrast computed tomography was the most sensitive and specific method among the diagnostic techniques used in this case.

Adult↗
PubMed1986

Neurotensin stimulates pancreatic exocrine secretion in rats.

Neurotensin (NT) stimulates pancreatic exocrine secretion in dogs and humans. The purpose of this study was to examine the effect of exogenous neurotensin on pancreatic exocrine secretion in rats. Five Sprague-Dawley male rats were prepared with pancreatic, gastric and duodenal fistulas. Bile was shunted into the duodenum in order to collect pure pancreatic juice. 24 h later, neurotensin (0.05, 0.1, 0.2, 0.3, 1.0 nmol/kg) was infused intravenously in a random fashion. Pancreatic juice was collected every 10 min, and the volume was recorded and protein and bicarbonate were measured. Neurotensin stimulated, in a dose-related manner, the pancreatic secretion of water, protein and bicarbonate. Neurotensin may be involved in the physiologic control of pancreatic secretion in rats.

Animals↗
PubMed1986

Effects of a thromboxane synthetase inhibitor (OKY-046) and a lipoxygenase inhibitor (AA-861) on bronchial responsiveness to acetylcholine in asthmatic subjects.

The effect of a selective thromboxane synthetase inhibitor, OKY-046, and a selective 5-lipoxygenase inhibitor, AA-861, on bronchial responsiveness to acetylcholine was studied in 23 asthmatic subjects. The provocative concentration of acetylcholine producing a 20% fall in forced expiratory volume in one second (PC20 FEV1) was measured before and after oral administration of OKY-046 (3000 mg over four days) and AA-861 (1100 mg over four days) and inhalation of OKY-046 (30 mg) in 10, 10, and nine asthmatic subjects respectively. Baseline values of FEV1 and forced vital capacity (FVC) were not altered by oral OKY-046, oral AA-861, or inhaled OKY-046. The geometric mean value of PC20 FEV1 increased significantly from 0.55 to 2.24 mg/ml after oral OKY-046, but was unchanged after inhalation of OKY-046 and after oral administration of AA-861. These results suggest that thromboxane A2 may play a part in bronchial hyperresponsiveness to acetylcholine.

Acetylcholine↗
PubMed1986

Additive effects of isoproterenol-phenylephrine aerosol following ipratropium bromide on airway obstruction in older patients with intrinsic asthma and chronic bronchitis.

The additive bronchodilating effect of isoproterenol-phenylephrine aerosol following ipratropium bromide was examined in seven intrinsic asthmatic patients and seven chronic bronchitic patients. FVC, FEV1 and Zrs were measured before and 30 min. after inhalation of ipratropium, 40 micrograms. Then inhalation of isoproterenol, 600 micrograms and phenylephrine, 570 micrograms was added and the pulmonary functions were measured 30 min. later. The age, baseline values of FVC and FEV1, and the increases in FEV1 and 1/Zrs with ipratropium did not differ between the two. Isoproterenol-phenylephrine aerosol following ipratropium produced further increases in FEV1 and 1/Zrs in asthmatic patients but no additive increases in bronchitic patients. These findings indicate that the role of autonomic nervous system, especially adrenergic system, on airway obstruction may be different between asthmatic and bronchitic patients and the method applied in this study may be helpful in differentiating these airway disorders.

Aerosols↗