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Y Wada

Publications and source records attributed to Y Wada.

At least 1,009 records · Page 56Linked to original sources

Differential effects of Bay k 8644, a presumed calcium channel activator, on sinoatrial nodal and ventricular automaticity of the dog heart.

Bay k 8644 is suggested to increase calcium influx through the voltage-dependent calcium channel. In isolated, blood-perfused sinoatrial node preparations of the dog. Bay k 8644 injected intra-arterially increased sinus rate as isoprenaline did. In isolated, blood-perfused papillary muscle preparations of the dog isoprenaline injected intra-arterially increased both the force of contraction of the papillary muscle and its spontaneous beating rate. In these preparations, however, Bay k 8644 failed to increase the beating rate, although it increased the force of contraction. These results are consistent with the concept that the slow inward current plays a role in sinoatrial nodal automaticity but not in automaticity of Purkinje fibres which was reflected as ventricular automaticity of the papillary muscle preparations used here.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

Involvement of contractile protein in hypotonic expansion of macrophages.

The volume measurement of macrophages from rabbit lungs was carried out using an automatic computerized cell counter. The size of freshly prepared macrophages was 669 +/- 62 fl at 4 degrees C. The cell volume increased gradually when the cells were suspended in an isotonic saline solution. Cytochalasin B initially enhanced the increase in cell volume but then caused a reduction. The reduction was considered to be due to structural changes in filament network of contractile proteins. Under hypotonic conditions, cytochalasin B-treated cells showed increased osmotic fragility and reduced expansibility. The increased fragility was considered to result from impairment of the network structure. These findings of the effect of cytochalasin B on the volume change suggest that contractile proteins play a protective role in the membrane against hypotonic expansion.

Animals↗

In vitro effects of estradiol, testosterone or progesterone on luteal steroidogenesis in the pregnant rat.

In order to assess the direct luteotropic effects of steroids, dispersed luteal cells from rats on day 8 or 16 of pregnancy were incubated for 2 h with various concentrations of estradiol (1-1000 ng/ml), testosterone (1-100 ng/ml) or progesterone (1-100 ng/ml). Estradiol, at any concentration, did not cause significant changes in the in vitro accumulation of progesterone, 20 alpha-dihydroprogesterone (20 alpha-OHP) or testosterone by dispersed luteal cells on both days 8 and 16. Addition of testosterone (1-100 ng/ml) increased the accumulation of estradiol on day 8 with estrone synthesized at half to one third the rate of estradiol. On day 16, accumulation of estradiol by dispersed luteal cells was more sensitive to 1 ng/ml testosterone than on day 8 with a concomitant drop in estrone synthesis. Although luteal secretion of estradiol was readily stimulated by testosterone, there were no corresponding changes in the production of progesterone or 20 alpha-OHP. Although the addition of a small amount of progesterone did not cause the anticipated increase in accumulation of 20 alpha-OHP, 100 ng/ml progesterone elicited a slight but significant increase in accumulation of 20 alpha-OHP on day 8. Thus, none of 3 steroids added was found to exert any direct in vitro luteotropic action in the pregnant rat, in acute experiments.

Animals↗

Comparison of in-vitro production of progestagens by the corpora lutea of early pregnancy of the rat and hamster.

Immature rats and adult hamsters were killed on Days 2, 4 or 8 of pregnancy (Day 1 = sperm positive vaginal smear). Dispersed luteal cells (5 X 10(4) cells) were incubated for 2 h in the absence or presence of graded doses of ovine LH. In the absence of LH, incubation of rat luteal cells compared to hamster cells produced about 3-6-fold as much progesterone, 26-66 times as much 20 alpha-dihydroprogesterone and about the same amounts of 17 alpha-hydroxyprogesterone. For the rat, 1 ng LH was the minimal dose which stimulated synthesis of progesterone and 17 alpha-hydroxyprogesterone by luteal cells on Days 2 and 4 whereas 10 ng LH stimulated maximal production of progesterone by Day-8 luteal cells. As pregnancy progressed from Day 2 to Day 8, there was an inverse relationship between the levels of progesterone and 20 alpha-dihydroprogesterone accumulated by rat luteal cells. For the hamster, 1 ng LH significantly stimulated accumulation of progesterone and 17 alpha-hydroxyprogesterone by Day-2 luteal cells but not by Day-4 or Day-8 cells. Hamster luteal cells on Day 4 produced the highest levels of progesterone in response to 10 or 100 ng LH, with a maximal rate of accumulation by Day-8 cells with 10 ng LH.

17-alpha-Hydroxyprogesterone↗

Presence of connectin-like protein in white blood cells and platelets.

Connectin is known to be an anchoring protein of actomyosin filaments in skeletal muscle. Attempts were made to extract this protein from white blood cells and platelets in order to investigate its properties. The purified connectin-like protein obtained had a rubbery appearance and was insoluble in water and immobile on SDS gel-electrophoresis. Amino acid composition and electron microscopic features of the protein were similar to those of skeletal muscles. FITC-labeled antibody to the protein showed a positive reaction to the membrane fractions of red cells, white cells and platelets. In moving cells fluorescence was observed not only in pseudopod, but also in whole cytoplasm. No changes in the fluorescence patterns were observed with respect to moving stages or cell types. The presence of the protein beneath the cell membrane was also confirmed electron micrographically.

Amino Acids↗

Cephabacins, new cephem antibiotics of bacterial origin. III. Structural determination.

The structures of 15 new cephem antibiotics, cephabacin F1-9 and H1-6, were determined by their spectroscopic analyses and decomposition studies. They are consisted of a cephalosporin nucleus and a di, tri or tetrapeptide including a new amino acid which is bound at the position 3 with an ester bond. The components, F1-9, showed unique biological activities by the presence of a formylamino group at the position 7.

Cephalosporins↗

Mode and mechanism of action of 3,4-dihydro-6-[4-(3,4-dimethoxybenzoyl)-1-piperazinyl]-2(1H)- quinolinone (OPC-8212), a novel positive inotropic drug, on the dog heart.

Mode and mechanism of action of 3,4-dihydro-6-[4-(3,4- dimethoxybenzoyl )-1-piperazinyl]-2(1H)- qu inolinone ( OPC -8212) were investigated exclusively on dogs both in vivo and in vitro. When assessed by intra-arterial administration in isolated, blood-perfused papillary muscle, sinoatrial node and atrioventricular (AV) node preparations, OPC -8212 produced a positive inotropic effect scarcely causing either positive or negative chronotropic and coronary vasodilator effects. AV nodal conduction was slightly facilitated with OPC -8212, whereas ventricular automaticity was rather suppressed. No arrhythmias were produced. Thus, OPC -8212 is highly specific for force. In heart-lung preparations OPC -8212 improved cardiac function depressed with pentobarbital, and caused bradycardia. In trabecular muscles of the right ventricle (hereafter simply called ventricular muscles) OPC -8212 produced a concentration-dependent positive inotropic effect in the presence of the beta 1-adrenoceptor antagonist, atenolol. This indicates that the positive inotropic effect of OPC -8212 is not mediated through a beta-adrenoceptor mechanism. In ventricular muscles OPC -8212 increased plateau potentials of normal action potentials in the presence of atenolol. In K+-depolarized ventricular muscles OPC -8212 increased overshoot potentials and durations of slow response action potentials in the presence of atenolol. These suggest an increase in the slow inward current to underlie the positive inotropic effect of OPC -8212. In ventricular muscles OPC -8212 shortened total duration of contraction and time to peak tension in the presence of atenolol. In ventricular muscles OPC -8212 increased force of contraction and intracellular concentrations of cyclic AMP in a parallel way in time course in the presence of atenolol.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Cardiovascular actions of the dihydropyridine calcium antagonist nimodipine in the dog.

When injected i.v. into anaesthetized, open-chest dogs, isopropyl (2-methoxyethyl)-1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3, 5-pyridinedicarboxylate (nimodipine, Bay e 9736) (0.3-10 micrograms/kg) produced an increase in coronary sinus outflow and decreases in mean arterial blood pressure, coronary resistance, arterio-venous oxygen difference and heart rate in a dose-dependent manner, but virtually no change in myocardial oxygen consumption. At 3 micrograms/kg i.v. of the drug coronary resistance fell nearly to half the pre-drug value, coronary sinus outflow nearly doubled and heart rate decreased by about 10 beats/min. Myocardial oxygen consumption was slightly reduced at 30 micrograms/kg i.v. and atrioventricular (AV) conduction time was slightly increased at 10 and 30 micrograms/kg i.v. of the drugs. When the coronary vascular and cardiac effects of nimodipine were assessed in isolated, blood-perfused dog heart preparations, i.e., sinoatrial node, AV node and papillary muscle preparations, by intra-arterial administration, the following was revealed. In nearly twice the dose doubling coronary arterial blood flow, nimodipine produced a 15% decrease in sinus rate and a 15% increase in AV conduction time. However, in reducing the force of contraction of the papillary muscle by half the pre-drug value was needed nearly 17 times the dose of nimodipine doubling coronary arterial blood flow. Suppression of AV conduction by large doses of nimodipine was evident only when it was injected into the artery supplying the AV node but not into the artery supplying the His-Purkinje-ventricular system.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗