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Biomedical subjects

I Matsubara

Publications and source records attributed to I Matsubara.

At least 55 records · Page 3Linked to original sources
PubMed1981

Effects of hyperosmotic solutions on the filament lattice of intact frog skeletal muscle.

The effect of increasing the osmotic strength of the extracellular solution on the fifament lattice of living frog sartorius and semitendinosus muscle has been studied using low-angle x-ray diffraction to measure the lattice spacing. As the extracellular osmotic strength is increased, the filament lattice shrinks like an osmometer until a minimal spacing between the thick filaments is reached. This minimal spacing varies from 20 to 31 nm, depending on the sarcomere length. Further increase in the osmotic strength produces little further shrinkage. The osmotic shrinkage curve indicates, for both muscles, an osmotically-inactive volume of approximately 30% of the volume in normal Ringer's solution. Shrinkage appears to be independent of temperature and the type of particle used to increase the osmotic strength (glucose, sucrose, small ions). The rate at which osmotic equilibruim is reached depends on muscle size, being slower for greater muscle diameters. Equilibrium spacings are approached exponentially with time constants ranging from 20 to 60 min. Independent of osmotic equilibrium, the lattice tends to shrink slowly by approximately 3% over the first few hours after dissection, probably because of a leakage of K+ ions from inside the muscle cells. This can be partly prevented by using an extracellular solution which contains a higher concentration of K+ ions or which is hypoosmotic. The volume of the muscle filament lattice (1.155d10(2) . S) is constant over a very wide range of sarcomere lengths, and is equal to approximately 3.6 x 10(6) nm3 for a range of amphibian muscle types.

Animals↗
PubMed1981

[Pharmacological studies on antispasmodics. IV. Ganglion blocking activity of 3-(di-2-thienylmethylene)-5-methyl-trans-quinolizidinium bromide (HSR-902) and the correlation between its blocking activity and its inhibitory activity towards urinary bladder contraction (author's transl)].

The ganglion blocking activity of HSR-902, a new antispasmodic agent, was compared with those of atropine sulfate, butylscopolamine bromide, timepidium bromide, prifinium bromide and hexamethonium chloride. These agents inhibited the postganglionic action potential induced by preganglionic cervical sympathetic nerve stimulation in cat and the order of potency was as follows: hexamethonium chloride much greater than timepidium bromide in equilibrium with butylscopolamine bromide greater than prifinium bromide greater than HSR-902 much greater than atropine sulfate. Moreover, the inhibitory activities were correlated with the inhibitory activities of these agents on urinary bladder contraction induced by pelvic nerve stimulation in cat which had been demonstrated in a previous report. On the nictitating membrane contraction induced by postganglionic cervical sympathetic nerve stimulation in cat, HSR-902 alone exhibited a slight inhibition. HSR-902, as well as tolazoline hydrochloride, an alpha-blocking agent, shifted the dose-response curve of noradrenaline-contraction in parallel to the right without decreasing maximal response in the isolated aorta of guinea pig, and the plots of Schild were found to be linear. These results suggested that the weak inhibitory activity of HSR-902 on urinary bladder contraction would be due to the weakness of its ganglion blocking activity and that it is a new antispasmodic agent with a slight alpha-blocking activity.

Action Potentials↗
PubMed1981

[Pharmacological studies on antispasmodics. V. Effect of 3-(di-2-thienylmethylene)-5-methyl-trans-quinolizidinium bromide (HSR-902) on the junctional transmission of pelvic nerve ending in isolated urinary bladder (author's transl)].

Effects of HSR-902, a new antispasmodic agent, on the junctional transmission of pelvic nerve ending in isolated urinary bladder was compared with those of atropine sulfate, butylscopolamine bromide, timepidium bromide and prifinium bromide. Tetrodotoxin (3 x 10(-8)g/ml) completely inhibited the contraction of isolated guinea pig urinary bladder induced by transmural stimulation (TM contraction), but hexamethonium chloride (1 x 10(-4)g/ml) and atropine sulfate (1 x 10(-5)g/ml) exhibited no inhibition and a slight inhibition, respectively. Neostigmine bromide (1 x 10(-7)g/ml) increased TM contraction, and the effect was completely inhibited by atropine sulfate (1 x 10(-5)g/ml). Antispasmodic agents (1 x 10(-7) - 1x 10(-5)g/ml), excluding HSR-902, showed slight inhibition on TM contraction. In contrast, HSR-902 (1 x 10(-6) - 1x10(-5)g/ml) increased TM contraction and/or resting tone (1 x 10(-5)g/ml). Phenoxybenzamine hydrochloride (1 x 10(-8)g/ml) and tolazoline hydrochloride (1 x 10(-5)g/ml), alpha-blocking agents, increased both TM contraction and resting tone. Increasing effects of HSR-902 on TM contraction and/or resting tone were completely inhibited by noradrenaline (1 x 10(-5)g/ml) with propranolol hydrochloride (1 x 10(-5)g/ml). These results suggested that these antispasmodic agents scarcely inhibited the junctional transmission in postganglionic cholinergic nerve ending induced by transmural stimulation of isolated guinea pig urinary bladder, and HSR-902 rather increased the transmission. Since it was also suggested that there was alpha-adrenoceptor inhibiting acetylcholine-release in the postganglionic cholinergic nerve terminal, the transmission increasing action of HSR-902 would be due to its alpha-blocking action.

Animals↗
PubMed1981

[Study of platelet aggregation by the filtration pressure method (author's transl)].

Using Hornstra's "filter loop" technique, effects of prostaglandins and vasodilators on ADP-induced platelet aggregation were studied in anaesthetized dogs. ADP-induced platelet aggregation was observed as a transient, reversible elevation of pressure before filter. This pressure change was reproducible and dose-related. PGI2 and PGE1 suppressed the elevation of pressure induced by ADP and decreased the spontaneous elevation of pressure. Thus, it was reconfirmed that PGI2 and PGE1 not only suppressed ADP-induced platelet aggregation but also produced a disaggregation of aggregated platelets. AFter indomethacin, ADP-induced platelet aggregation was potentiated and sometimes became exceedingly protracted, indicating that anti-aggregatory prostaglandin was always present in the circulating blood. Close-injection of bradykinin did not suppress ADP-induced platelet aggregation, while intravenous injection did produce a suppression. After indomethacin, this inhibitory effect was greatly attenuated, indicating a release of anti-aggregatory prostaglandin (PGI2?) by bradykinin. Coronary vasodilators, such as dipyridamole and nifedipine did not inhibit ADP-induced platelet aggregation, nor did sulfinpyrazone. It is concluded that the "filter loop" technique is a useful method that allows aggregation and disaggregation reactions to be followed continuously and quantitatively in the blowing blood. The effects of drugs on platelet aggregation can be assessed in connection with hemodynamic changes such as blood pressure and heart rate induced by systemic administration of the drugs.

Adenosine Diphosphate↗
PubMed1981

[Pharmacological studies of antispasmodics. III. Antispasmodic activity of 3-(di-2-thienylmethylene)-5-methyl-trans-quino-lizidinium bromide (HRS-902) on smooth muscle organs and its organ selectivity (author's transl)].

Pharmacological activities of HSR-902, a new antispasmodic agent, in gastrointestinal tract, biliary and urinary systems were compared with those of atropine, butylscopolamine bromide, timepidium bromide, prifinium bromide and diphemanil methylsulfate. In isolated smooth muscle organs (stomach, duodenum, ileum, colon, gall bladder and urinary bladder), anti-acetylcholine activities of HSR-902 were the most potent among these agents but its activity in urinary bladder, similar to findings in the cases of atropine and diphemanil methylsulfate, was relatively less potent than that of prifinium bromide, timepidium bromide and butylscopolamine bromide. Regarding the contractions of stomach, jejunum and ileum, which were induced by vagus nerve stimulation or acetylcholine, and on the ileum spontaneous motility, antispasmodic activities of HSR-902 were almost equal to or somewhat more potent than those of atropine, and its activities were more potent than those of prifinium bromide, timepidium bromide, diphemanil methylsulfate and butylscopolamine bromide. On the gall bladder pressure and the counts of perfusion through Oddi's Sphincter, these agents exhibited a similar inhibition and enhancement, respectively. In the case of urinary bladder contractions induced by pelvic nerve stimulation, these agents exhibited a weak inhibition. The inhibitory effect of HSR-902 was relatively less potent than that of other agents except atropine, which had little effect. HSR-902 was similar to atropine in this so-called "atropine-resistance".

Acetylcholine↗
PubMed1980

Myosin heads do not move on activation in highly stretched vertebrate striated muscle.

Highly stretched muscles in which thick and thin filaments no longer overlap produce little or no tension on activation. In preparations producing no tension, the 42.9-nanometer myosin layer line shown in x-ray diffraction patterns does not become weaker. This suggests that myosin heads do not move from their resting positions in the absence of actin.

Actins↗
PubMed1980

Cardiotoxic effects of 5-fluorouracil in the guinea pig.

In order to search into the underlying mechanisms of ECG changes suggestive of ischemia observed in humans and in rabbits after administration of 5-fluorouracil (5-FU), experiments were performed in anesthetized open-chest guinea pigs. The substance produced similar ECG changes in this species as well, after a rather long latent period of around 3 hours after intravenous administration. The incidence of ECG abnormality in animals given 60 mg/kg was 7/7, while that in animals given 30 mg/kg was 4/9. with 10-20 mg/kg, ECG changes were not observed during an experimental period as long as 5 hours. Associated with these ECG changes, a depletion of the high-energy phosphate compounds of the ventricular myocardium was observed. Analysis of tricarboxylic acid cycle (TCA cycle) intermediates revealed an accumulation of citrate within the myocardium, suggesting a malfunction of TCA cycle resulting from an inhibition of aconitase by fluorocitrate, as a cause of depletion of the high-energy phosphates. It is highly probable that the accumulation of citrate was due to the formation of fluoroacetate, an inhibitor of aconitase, from 5-FU via alpha-fluoro-beta-alanine, a major degradation product of 5-FU, for it is known that beta-alanine is usually converted to acetate.

Adenosine Diphosphate↗
PubMed1980

Effects of prostacyclin on platelet aggregation as studied with "filter-loop" technique in the flowing blood of the dog.

Using Hornstra's "filter loop" technique for determination of platelet aggregation in the circulating blood, the role played by prostaglandin I2 (PGI2) in platelet aggregation was studied in the canine heart-lung preparation (HLP) supported by a donor. A dose-related aggregation of platelet was induced by close injection of ADP into the "filter loop". PGI2 induced a marked suppression of ADP-induced platelet aggregation. After indomethacin, ADP-induced platelet aggregation became very much protracted, but was promptly terminated by PGI2. Bradykinin produced an inhibition of platelet aggregation, while it produced an increase in the coronary blood flow (CBF). After indomethacin, the increase in CBF and the inhibition of ADP-induced platelet aggregation produced by bradykinin was greatly attenuated. Essentially similar results were obtained in the anesthetized closed-chest dogs. These findings strongly suggest that the transient nature of ADP-induced platelet aggregation in the flowing blood is due to the intervention of antiaggregatory PGI2.

Adenosine Diphosphate↗
PubMed1980

Pharmacological studies of 1-(2-chloro-4-hydroxyphenyl)-2-t-butylaminoethanol (HOKU-81), a new bronchodilator. 1st Communication: Bronchodilator and cardiovascular actions.

Bronchodilating action and influence on the cardiovascular system of 1-(2-chloro-4-hydroxyphenyl)-2-t-butylaminoethanol (HOKU-81), which is one of metabolites of tulobuterol obtained from rat urine, were examined using the isolated tracheae and atria of guinea pigs in vitro and dogs in vivo in comparison with those of the parent drug, i.e., tulobuterol isoprenaline, salbutamol and other reference bronchodilators. HOKU-81 was approximately 8 times more potent than tulobuterol, approximately twice as potent as salbutamol, and approximately as potent as isoprenaline in relaxing effect on the isolated tracheal smooth muscle preparation of guinea pigs. This effect of HOKU-81 seems to be due to direct action on the adrenergic beta-receptor. In anaesthetized dogs, bronchodilating effect of HOKU-81 was much more potent than that of tulobuterol and was approximately as potent as that of salbutamol when administered i.v., and its effect lasted for many hours. When administered orally, the duration of bronchodilating effect of HOKU-81 was almost as long as that of salbutamol. The cardiac stimulating effect of HOKU-81 examined in the isolated guinea pig artia and in anaesthetized dogs was weaker than those of isoprenaline and salbutamol, though stronger than that of tulobuterol. In the present studies in vitro as well as in vivo, the selectivity ratio of HOKU-81 for beta-adrenoceptors in the tracheal smooth muscle vs. those in the right atrial muscle was the largest of all the bronchodilators used.

Acetylcholine↗