Search PubMed⌕ Search

Biomedical subjects

H Satoh

Publications and source records attributed to H Satoh.

At least 721 records · Page 40Linked to original sources
PubMed1989

Possible mechanism for the inhibition of gastric (H+ + K+)-adenosine triphosphatase by the proton pump inhibitor AG-1749.

Mechanisms related to the inhibition of (H+ + K+)-adenosine triphosphatase (ATPase) by 2-[[[3-methyl-4-(2,2,2-trifluoroethoxy)-2-pyridyl]methyl] sulfinyl]-1H-benzimidazole (AG-1749) were studied using canine gastric microsomes. AG-1749 (1-100 microM) inhibited the K+-stimulated ATP hydrolysis and vesicular accumulation of H+. AG-1749 bound to the microsomes concentration-dependently and decreased the number of free SH groups; the binding correlating with the enzyme inhibition. Both the binding and inhibition were antagonized by dithiothreitol. N-ethylmaleimide inhibited the (H+ + K+)-ATPase and decreased the binding of [14C]AG-1749 to the microsomes. The inhibitory effect of AG-1749 gradually increased with incubation time, and was enhanced by lowering the pH. AG-2000 and AG-1812, acid-induced rearrangement products of AG-1749, inhibited (H+ + K+)-ATPase potently, rapidly and independently of pH; the inhibition was antagonized by dithiothreitol. We propose that AG-1749 is transformed into its active forms within the acidic compartment of the parietal cells and that the active compounds inhibit (H+ + K+)-ATPase activity by reacting with the SH groups of the enzyme.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1989

Antisecretory and antiulcer activities of a novel proton pump inhibitor AG-1749 in dogs and rats.

The antisecretory and antiulcer activities of 2[[[3-methyl-4-(2,2,2-trifluoroethoxy)-2-pyridyl]methyl] sulfinyl]-1H-benzimidazole (AG-1749) were investigated in dogs and rats. AG-1749 inhibited both the (H+ + K+)-adenosine triphosphatase activity in canine gastric microsomes and dibutyryl cyclic AMP-stimulated acid formation in isolated canine parietal cells and suppressed the acid secretion stimulated by histamine, pentagastrin, bethanechol or a peptone meal in Heidenhain pouch dogs; the ID50 values were between 0.2 and 0.7 mg/kg p.o. AG-1749 inhibited both the histamine-stimulated and the basal acid secretion in pylorusligated rats and prevented water immersion stress or aspirin-induced gastric lesions and mepirizole or cysteamine-induced duodenal ulcers in rats; the ID50 values were between 0.3 to 3.6 mg/kg p.o. or i.d. Furthermore, AG-1749 prevented gastric lesions induced by absolute ethanol or acidified aspirin, and accelerated the healing of acetic acid-induced gastric or duodenal ulcers in rats. The inhibitory potency of AG-1749 in dogs was much the same as that of omeprazole and about half that of ranitidine. However, it was about 2 to 10 times more potent than omeprazole and 4 to 34 times more potent than ranitidine in rats. These results suggest that AG-1749 exerts prominent antiulcer activities mainly by suppressing acid secretion via an inhibition of a proton pump in gastric parietal cells and partly by protecting the gastrointestinal mucosa against various ulcerative stimuli.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1989

[Brachiocephalic arterial aplasia of the right aortic arch with subclavian steal syndrome].

A 44-year-old man was admitted to our hospital with complaint of weakness in his left upper extremity, vertigo, and diplopia. After aortic root injection of contrast medium, a right aortic arch was visualized. The left brachiocephalic artery was not found, however. An operation was performed through a midline sternotomy. The first branch of the aortic arch was the right common carotid artery, and the second branch was the right subclavian artery. The left brachiocephalic arterial aplasia was recognized. An E-PTFE graft was anastomosed proximally to the ascending aorta and distally to the junction of the left common carotid and left subclavian arteries. After the operation, some of the symptoms were improved and the others were removed.

Adult↗
PubMed1989

[A case of isolated tricuspid regurgitation associated with protein-losing gastroenteropathy].

A 43 year old woman was admitted to our hospital in April 1987 due to shortness of breath and pedal edema. She had a history of sepsis associated with the crisis of hyperthyroidism 15 years prior to the admission. Physical examination revealed a badly nourished with ascites: weight was 56 kg and height 156 cm. The heart sounds were distant with mild holosystoric murmur (grade I/VI) at xiphoisternum. The chest X-ray showed cardiomegaly (CTR: 72.3%) with pleural effusion. The electrocardiogram showed atrial fibrillation, low voltage and right ventriculer hypertrophy. The echocardiogram showed marked dilatation of right atrium and ventricle with very short septal leaflet of tricuspid valve. The anterior and posterior leaflets were undetected. The tricuspid regurgitant doppler signal was recorded up to hepatic vein. No other abnormalities were noted in other valves. The white cell count was 4900 with lymphocytopenia (26%; T-cell 82%, B-cell 13%). Serum total protein was reduced to 3.4 g/dl with albumin 1.64 g/dl. Immunoelectrophoresis showed normal IgG, IgA and IgM. Proteinuria was not recognized. Fecal excretion of polyvinylpyrrolidone-131I (PVP) was elevated to 2.8%, The systolic pressure in pulmonary artery, right ventricle, right atrium, superior and inferior vena cave were almost equal as 26 mmHg. The pulmonary arterial scintigraphy disclosed multiple peripheral defects in both lungs. Two weeks after the operation of tricuspid valve replacement based on the diagnosis of protein-losing enteropathy due to isolated tricuspid regurgitation, serum total protein and albumin were normalized to 6.8 g/dl and 3.6 g/dl respectively, but the lymphocytopenia was persistent. She become very well, with free of ascites and edema.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Effects of indomethacin on cellular resistance and synthesis of prostaglandins in epithelial cells isolated from rat gastric mucosa].

This study was done to test effects of indomethacin (IND) on cell damage and prostaglandin (PG) synthesis in mucosal epithelial cells isolated from rat stomach in vitro. IND caused the cell damage in a dose-related way at concentrations over 5 X 10(-4) M. This damage was inhibited by 16,16-dimethyl PGE2 (10(-6) M). IND abolished the synthesis of PGE2, PGI2, and TXA2 at the concentration of 10(-4) M at which IND alone did not cause cell damage. The cells treated with 10(-4) M IND were significantly susceptible to damage caused by 15% ethanol compared to the cells not treated with IND. 16,16-Dimethyl PGE2 also inhibited the damage caused by IND + ethanol. These results suggest that the IND-induced susceptibility of the cells to damage is related to PG deficiency.

16,16-Dimethylprostaglandin E2↗
PubMed1989

Scanning electron microscopic study of periendothelial cells of the rat cerebral vessels revealed by a combined method of corrosion casting and KOH digestion.

A combined method of corrosion casting and KOH digestion was used for the scanning electron microscopic (SEM) observation of the external walls of the blood vessels running on the surface and in the parenchyma of the rat cerebral cortex. The plastic resin which was preliminarily injected into the cerebral vessels reinforced the preservation of the vessel walls during the chemical digestion. Using the present method, the walls of blood vessels running on the surface and in the parenchyma of the cerebral cortex were clearly seen with SEM. The arterioles showed a rich arrangement of smooth muscle cells embracing the external surface of the endothelia, and the venules had sparse, flat smooth muscle cells. The capillaries were surrounded by many pericytes which were extremely similar to those seen in the other organs of the animals. There were observed two different kinds of pericyte. One type of the pericytes in the present specimens extended very long cytoplasmic processes parallel to the long axis of the capillaries. Another type of the pericytes had relatively short, broad and flat cytoplasmic processes radiated to embrace the capillary walls. The former was frequently seen in the capillaries on brain surface and in the parenchyma, whereas the latter was relatively rare. The availability of the present method was also discussed in comparison with the previous descriptions.

Animals↗
PubMed1989

The effect of bispecific monoclonal antibody recognizing both hepatoma-specific membrane glycoprotein and anthracycline drugs on the metastatic growth of hepatoma AH66.

A monoclonal mouse antibody (MoHG) was produced using in vitro cultured AH66R tumor cells treated with cholesteryl hemisuccinate as an immunogen. The antibody identified a 90 kd membrane glycoprotein (HG-90) which is expressed on in vitro cultured hepatoma cell lines AH66 and AH66R. A monoclonal antibody was prepared to the anthracycline drug daunomycin, and it also reacted with adriamycin. A fusion was made of the hybridoma HG-90 with the hybridoma which recognized daunomycin/adriamycin. This bispecific hybridoma A8C recognized both determinants. We studied the therapeutic effect of the A8C bispecific antibody with adriamycin treatment and compared it to the effect of the bispecific antibody to which adriamycin had been conjugated via an albumin (Alb) bridge. The therapy model used was the tumor AH66R in Donryu rats. Tumor bearing rats had their subcutaneous tumors resected on day 10, a time when distant metastases were present. After the surgical resection of the tumor the rats were injected intravenously for two cycles with the bispecific antibodies, followed by the administration of adriamycin (ADR) or MoHG.Alb.ADR conjugates. A slight therapeutic effect occurred with either MoHG or ADR alone but treatment with the bispecific antibody followed by the administration of ADR or with the MoHG.Alb.ADR conjugates significantly prolonged survival, with 60% of the treated animals being "tumor free" when sacrificed on day 80. Lower serum concentrations of alphafetoprotein were observed with the bispecific antibody and drug treatment. This suggests that the bispecific antibody/drug treatment is potentially more beneficial in the suppression of distant metastases than the MoHG.Alb.ADR conjugate. This may be due to an increase in the local drug concentration of unmodified adriamycin.

Animals↗
PubMed1989

[Treatment of multiple myeloma with LAK cells plus interleukin 2 or interleukin 2 alone].

Three patients with multiple myeloma were treated with 3.3-10 x 10(5) u/day intravenous or subcutaneous IL 2 alone. Both their Leu7 and CD16 positive cells in the peripheral blood and NK and LAK cell activity elevated but no M protein decreased. LAK cells and IL-2 administered to three patients intravenously. Lymphocyte counts in the peripheral blood elevated remarkably in one patient and CD3, 8, 16, 2, 38, Leu7 positive cells and NK cell activity increased in three patients. Though the reduction of M proteins were observed in three patients (17%, 75.8% and 40%, respectively), they returned to pretreatment level in 35 days, 55 days and 200 days after the therapy. Significance of the therapy against multiple myeloma was discussed.

Aged↗
PubMed1989

[Protection by 16,16-dimethyl PGE2 of surface epithelial, parietal, and chief cells isolated from rat stomach].

Damage caused by ethanol and its prevention by 16,16-dimethyl PGE2 were tested in fractions rich in surface epithelial cells (F1), rich in chief cells (F2), and rich in parietal cells (F3) isolated from rat stomach in vitro. Ethanol caused cell damage in F1 in a dose-related way and the concentration of ethanol for induction of 50% cell damage was 14.93%. There was no difference in cell damage caused by 15% ethanol between the three different cell fractions. 16,16-Dimethyl PGE2 (10(-6)M) significantly inhibited the damage caused by 15% ethanol in all the three fractions. These results suggest that 16,16-dimethyl PGE2 has direct protective effect on gastric cells and this action is not limited to the specific cell type.

16,16-Dimethylprostaglandin E2↗
PubMed1989

An erythromycin derivative, EM-523, induces motilin-like gastrointestinal motility in dogs.

The effect of an erythromycin derivative, EM-523, on gastrointestinal motility was investigated in conscious dogs and compared with that of motilin cisapride, trimebutine and metoclopramide. In the fasting state, EM-523 given i.v. or i.d. at 3 micrograms/kg or more induced contractions in the stomach that migrated along the small intestine. The pattern of the contractions was very similar to that induced by motilin. In the digestive state, EM-523 increased the amplitude of gastric contractions. Cisapride and metoclopramide increased gastrointestinal motility both in the fasting and digestive states; however, their contractile pattern was different from that of EM-523. Trimebutine did not induce gastric motility in the fasting state but rather decreased gastric motility in the digestive state. The contractions induced by EM-523 and motilin were inhibited by atropine but were not affected by naloxone, suggesting that the cholinergic pathway is important in the exertion of their action. These results indicate that EM-523 mimics motilin in stimulating gastrointestinal motility and that this agent may be useful treat gastrointestinal disorders such as gastric stasis, gastroesophageal reflux, and postoperative ileus, and so forth.

Animals↗
PubMed1989

[A case of retrocecal appendicitis occurrence during effective chemotherapy in lung cancer].

Reported is the case of 61-year-old male patient who developed an abscess, secondary to a ruptured retrocecal appendicitis, while undergoing effective chemotherapy for lung cancer. Patients undergoing cancer chemotherapy are especially susceptible to infectious complications because chemotherapy can cause myelosuppression. To our knowledge, has been no previous reported case of retrocecal appendicitis occurring during chemotherapy for the lung cancer. Retrocecal appendicitis is a dangerous form of complication occurring in patients being treated with chemotherapeutic drugs.

Abscess↗
PubMed1989

[A clinical study of diltiazem administration using cold glucose-insulin-potassium cardioplegic solution--comparison between diltiazem cardioplegia and diltiazem pretreatment].

A recent idea of myocardial injury during open heart surgery is thought to be caused by the intracellular calcium overload. So, one possibility for improving myocardial protection is expected on the blocking agents of transmembrane calcium movements. This study was designed to clarify the effect of Diltiazem, a kind of calcium blocking agents, on myocardial protection in terms of hemodynamics and plasma Diltiazem concentration. 38 patients who underwent coronary artery bypass grafting using glucose-insulin-potassium cardioplegic solution (GIK) were divided into three groups Control (CO) group: no Diltiazem administration. Diltiazem cardioplegia (DC) group: GIK containing 7.5 mg/l Diltiazem was used. Diltiazem pretreatment (DP) group: Diltiazem was administered intravenously 1.5 micrograms/kg/min before operation to after operation continuously. Plasma Diltiazem concentration was constantly kept at about 150 ng/ml during 24 hours after surgery in DP. On the contrary, in DC, the level was very high (10,000 ng/ml) during aortic cross clamp but decreased about 50 ng/ml at 3 hours after surgery, and Diltiazem was not detected in CO. DC included many cases of bradycardia required pacing, however, it diminished as plasma concentration decreased. Aid of catecholamin administration was reasonable in three groups. DP and DC included many cases of commendable cardiac function in terms of cardiac index, systemic vascular resistance and left ventricular work during acute stage of surgery, and there were no coronary spasm and perioperative infarction. It is concluded that Diltiazem is effective to keep good cardiac function after reperfusion, and combined (Diltiazem pretreatment--1.5 micrograms/kg/min drip infusion-and Diltiazem cardioplegia-total dose 150-300 micrograms/kg) administration should be advisable.

Calcium Channel Blockers↗
PubMed1989

[Multiple cerebral infarction following coronary artery bypass grafting for the patient with calcified aorta--a case report].

The cardiac surgeon occasionally may encounter a diseased or rigidly calcified aorta in the patient requiring myocardial revascularization. In this paper, a 72-year-old woman who suffered from neurological injury following coronary artery bypass grafting due to embolization of atheromatous debris from the calcified ascending aorta was described. A review of the literature was also performed to emphasize the importance of the recognition, and management of the calcified and diseased ascending aorta.

Aged↗
PubMed1988

Human M2-type pyruvate kinase: cDNA cloning, chromosomal assignment and expression in hepatoma.

Two overlapping clones, covering the entire coding sequence of human M2-type pyruvate kinase (PK) cDNA, were isolated and sequenced. Nucleotide sequencing results showed that they contained the 109-bp 5'-untranslated region, the 1593-bp coding region and the 585-bp 3'-untranslated region. Nucleotide sequence homology was 90% and 69% with rat M2-type and L-type PK cDNA, respectively. In situ hybridization using the human M2-type PK cDNA probe disclosed that the gene for M2-type PK is located at band q22 on chromosome 15. Northern blot analysis with RNA from human hepatoma demonstrated that M2-type PK was predominantly expressed in hepatoma cells, whereas L-type PK was preferentially expressed in the non-tumor portion of the liver.

Amino Acid Sequence↗