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Biomedical subjects

M Ohura

Publications and source records attributed to M Ohura.

30 records · Page 2Linked to original sources
PubMed1991

Organic Ca(2+)-antagonist-resistant response to FMRF-NH2 on the molluscan smooth muscle.

1. FMRF-amide (10(-7)-10(-5) M) contracted molluscan anterior byssus retractor muscle in a concentration-dependent fashion. 2. The concentration-response curve of FMRF-amide was shifted rightward by an analogue of FMRF-amide, FMRf-amide ([D-Phe4]FMRF-amide, putative FMRF-amide receptor antagonist) in a parallel manner (pA2 = 4.87 +/- 0.04). 3. Although a contractile response to KCl was reduced by the organic Ca2+ antagonists (verapamil, diltiazem and high concentration of nifedipine and nicardipine). FMRF-amide-induced contraction was not markedly reduced by them. 4. In the Ca(2+)-free medium, FMRF-amide-induced contraction was diminished. The response was also reduced by TMB-8 (10(-4) M), suggesting that FMRF-amide-induced contraction might be partly dependent on intracellular Ca2+. 5. An inorganic Ca(2+)-antagonist, MnCl2, markedly reduced the FMRF-amide- and KCl-induced contraction. The results show that FMRF-amide-induced contraction might be dependent on extracellular Ca2+. 6. These findings suggest that FMRF-amide-induced contraction might be mediated through an action on FMRF-amide receptors and not through the activation of organic Ca2+ antagonist-sensitive Ca2+ channels.

Animals↗
PubMed1991

Ischemic preconditioning preserves creatine phosphate and intracellular pH.

BACKGROUND: Ischemic preconditioning slows ATP depletion and ultrastructural damage during the final episode of ischemia. To define the influence of creatine phosphate (CP) and intracellular pH (pHi) on this effect, CP and pHi were serially measured in porcine hearts without collateral circulation by using 31P-NMR spectroscopy and ultrastructural examination. METHODS AND RESULTS: Farm pigs weighing 12-15 kg were anesthetized with Fluothane. The control group underwent a single occlusion (20 minutes or 60 minutes); the preconditioned group underwent four episodes of 5-minute occlusion and 5-minute reperfusion followed by a sustained occlusion (20 minutes or 60 minutes). After ischemic preconditioning, CP increased to 115 +/- 11% (p less than 0.05) of preischemic value and ATP decreased to 84 +/- 8% (p less than 0.05) of preischemic value, but pHi returned to preischemic value. At 5 and 10 minutes of sustained ischemia, CP was significantly preserved in the preconditioned group (control group, 19 +/- 3% versus preconditioned group, 29 +/- 4% at 5 minutes; control group, 5 +/- 3% versus preconditioned group, 11 +/- 3% at 10 minutes; p less than 0.05). At 15 and 20 minutes of sustained ischemia, ATP was significantly preserved in the preconditioned group (control group, 64 +/- 3% versus preconditioned group, 73 +/- 3% at 15 minutes; control group, 51 +/- 7% versus preconditioned group, 62 +/- 2% at 20 minutes; p less than 0.05). At 10, 15, 20, and 25 minutes of sustained ischemia, pHi was significantly higher in the preconditioned group (control group, 6.5 +/- 0.05 versus preconditioned group, 6.7 +/- 0.1 at 10 minutes; control group, 6.3 +/- 0.05 versus preconditioned group, 6.6 +/- 0.06 at 15 minutes; control group, 6.1 +/- 0.1 versus preconditioned group, 6.4 +/- 0.1 at 20 minutes; control group, 6.0 +/- 0.2 versus preconditioned group, 6.3 +/- 0.1 at 25 minutes; p less than 0.05). Ultrastructural changes were milder in the preconditioned group at 20 minutes of sustained ischemia. CONCLUSIONS: In addition to ATP and ultrastructure, preconditioning preserved CP and pHi during sustained ischemia. These protective effects might be due to overshoot phenomenon of CP and/or reduced ATP consumption. The relatively longer period of preservation of pHi, which probably is the result of reduced ATP consumption, indicates its greater contribution to reducing infarct size than that of CP and ATP.

Adenosine Triphosphate↗
PubMed1990

Protective effect of verapamil in ischemic porcine hearts: analysis of ultrastructural and metabolic changes using in vivo 31P-NMR spectroscopy.

To assess the protective effect of verapamil on ischemic myocardium, the changes in high energy phosphates, inorganic phosphate, and intracellular pH were serially and quantitatively measured in ischemic porcine hearts without collateral circulation using 31P-NMR spectroscopy, together with ultrastructural examination. Twenty-six farm pigs weighing 11 to 14 kg were anesthetized with fluothane and were divided into control (C) group and verapamil pretreatment (V) group. In V group 0.2 mg/kg of verapamil was administered for 20 mins before occlusion of the anterior descending coronary artery. 31P-NMR spectra were serially obtained throughout the experiment, and ultrastructural examination was done at 20-min occlusion and at 120-minute occlusion in each group. At 10-min ischemia, creatine phosphate was significantly preserved in V group (C/V = 11 +/- 4%/16 +/- 5% P less than 0.05). At 20 min ischemia, ATP was significantly preserved (C/V = 60 +/- 9%/73 +/- 8% P less than 0.05), and intracellular pH was significantly higher in V group (C/V = 6.4 +/- 0.2/6.6 +/- 0.1 P less than 0.05). Morphologically, clumping of the nuclear chromatin, mitochondrial swelling and decrease in glycogen were milder in V group at 20 min ischemia. However, these beneficial effects disappeared at 120 min ischemia. Thus pretreatment with verapamil attenuated depletion of high energy phosphates, progression of acidosis, and ultrastructural changes. There was no significant difference of rate pressure product and regional blood flow between hearts with and without pretreatment of verapamil. Therefore, this protective effect may be due to the energy sparing effect or other direct subcellular effect of verapamil on ischemic myocyte.

Angiography↗
PubMed1990

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Journal Article↗
PubMed1988

Effects of bile salts on plasma concentration of beta-endorphin-like immunoreactivity in men.

The effects of bile salts on the release of beta-endorphin-like immunoreactivity (beta-END-LI) were investigated in men using a specific radioimmunoassay developed by the authors. Plasma beta-END-LI was determined after extraction by the acid-acetone method (recovery: 73 +/- 5%). Oral administration of 400 mg of sodium taurocholate caused a rise in plasma beta-END-LI from 9.9 +/- 0.5 pmol/liter to 21.3 +/- 1.2 pmol/liter after 30 min and 18.1 +/- 0.5 pmol/liter after 60 min, with return to the initial value after 90 min. Oral administration of chenodeoxycholic acid (CDCA) also increased plasma beta-END-LI from a basal level of 8.4 +/- 0.7 pmol/liter to 18.7 +/- 0.8 pmol/liter after 30 min. Oral administration of ursodeoxycholic acid (UDCA) increased plasma beta-END-LI from 7.3 +/- 0.3 pmol/liter to 30.6 +/- 0.2 pmol/liter after 30 min. In gel chromatography, the beta-END-LI released after UDCA administration separated into two components, which eluted in the same positions as human beta-lipotropin and human beta-endorphin, respectively. These results suggested that bile salts may participate the release of beta-END-LI.

Administration, Oral↗
PubMed1986

An elevated type of gastric ulcer scar in patients treated with cimetidine.

An elevated type of gastric ulcer scar (EUS) (A) was noted in 8 out of 227 ulcer patients treated with cimetidine. These were compared with 15 patients with EUS (B), not treated with cimetidine and the etiology of the lesion was discussed. The incidence of EUS (3.5%) and the average age of the patients were higher (61 years) in the A group than in the B group. The scar was seen all over the stomach in the A group. The period from detection of gastric ulcer to confirmation of EUS averaged 4 weeks, and there was no difference between the two groups. No difference was seen in the histological findings of elevated lesions either. In the A group, it appears that EUS was induced by rapid tissue regeneration due to the strong anti-ulcer effect of cimetidine in ulcer lesions, since it was noted in the regions where it had previously been considered unlikely to occur.

Adolescent↗
PubMed1985

In vivo and in vitro effects of bradykinin on the release of beta-endorphin-like immunoreactivity.

The effect of bradykinin (BK) on the release of beta-endorphin-like immunoreactivity (beta-EpLI) in rats was studied in vivo and in vitro. Intraperitoneal injection of BK at 5 micrograms/100 g body weight resulted in significant increase in the plasma beta-EpLI level after 15 min. BK at concentrations of 10(-12)-10(-7) M also caused dose-dependent stimulation of beta-EpLI release from dispersed cells of rat anterior pituitary. On gel chromatography, the beta-EpLI released by incubation of the cells with 10(-7) M BK separated into two components, eluted in the same positions as human beta-lipotropin and human beta-endorphin, respectively. BK did not stimulate beta-EpLI release in Ca++-free medium. Addition of 10(-3) M verapamil or 10(-6) M dexamethasone to the incubation medium inhibited BK-induced beta-EpLI release from the cells. Quabain (10(-5) M) also stimulated beta-EpLI release, but its effect was not additive with that of BK. These results indicate that BK stimulates beta-EpLI release and that calcium ion is involved in the mechanism of this effect.

Animals↗
PubMed1984

Postprandial release of neurotensin-like immunoreactivity and its mechanism.

The effects of various ingested materials on plasma neurotensin-like immunoreactivity (NTLI) in humans were investigated using a newly developed, specific radioimmunoassay. Plasma NTLI was determined after its extraction with acid/acetone (recovery 77 +/- 4%). The intraassay and interassay coefficients of variation were 3.6% and 8.9%, respectively. The plasma concentration of human NTLI in normal subjects was 5.6 +/- 2.9 pmol/l and showed no significant sex difference. Ingestion of a test meal (150 g of Campbell's condensed meat soup) caused a biphasic rise in plasma NTLI from a basal level of 5.7 +/- 1.0 pmol/l to 10.8 +/- 1.2 pmol/l after 30 min and 9.6 +/- 1.1 pmol/l after 120 min. Ingestion of 5.5 g fat resulted in a biphasic rise in plasma NTLI from a basal level of 4.8 +/- 0.3 pmol/l to 8.9 +/- 0.3 pmol/l after 15 min and 11.9 +/- 0.4 pmol/l after 90 min. When 100-150 mg of ileal mucosa was perfused with a solution of 2 mEq/l fatty acids, 1 mM or 5 mM sodium taurocholate or 154 mM sodium bicarbonate (NaHCO3), the release of NTLI from the mucosa into the perfusate was 2.3-fold, 4.3-fold and 7.5-fold, respectively, over the base level. These results indicate that NTLI release is stimulated by ingestions of meat soup and fat and that NTLI present in the human ileum is released by the direct actions of solutions of fatty acid, sodium taurocholate, and NaHCO3 on the ileal mucosa. These findings strongly suggest that neurotensin (NT) has a physiological role in gut physiology.

Adult↗
PubMedDate not supplied

Cardiovascular effects of OPC-13340, a potent, long-acting 1,4-dihydropyridine calcium channel blocker, in dogs.

The cardiovascular effects of OPC-13340, a newly developed 1,4-dihydropyridine calcium channel blocker, were examined in several canine preparations. In conscious normotensive and DOCA-salt hypertensive dogs, OPC-13340, at doses of 10 to 30 micrograms/kg, i.v., and 0.3 to 3 mg/kg, p.o., exerted an hypotensive action in a dose-dependent manner. The hypotensive action of OPC-13340 was longer lasting and more potent than that of nicardipine and nifedipine. In conscious, normotensive instrumented dogs, OPC-13340, at doses of 1 and 3 mg/kg, p.o., dose-dependently decreased total peripheral resistance and mean blood pressure and increased heart rate, cardiac output and left ventricular contractility. In anesthetized open-chest dogs, OPC-13340, at doses of 1 to 30 micrograms/kg, i.v., increased coronary blood flow and decreased mean blood pressure, heart rate, coronary vascular resistance, arteriovenous oxygen difference and myocardial oxygen consumption. In contrast to OPC-13340, nicardipine did not change the myocardial oxygen consumption. From these results it was concluded that OPC-13340 lowered blood pressure and improved coronary circulation in dogs and that the duration of these actions was longer lasting than that of nifedipine and nicardipine. These actions of OPC-13340 may be useful in the treatment of hypertension and angina pectoris.

Anesthesia↗