PubMed Health⌕ Search

Biomedical subjects

N Taira

Publications and source records attributed to N Taira.

At least 199 records · Page 11Linked to original sources
PubMed1982

Positive inotropic effect of amrinone in relation to cyclic nucleotide metabolism in the canine ventricular muscle.

Experiments were carried out in the canine isolated right ventricular muscle in order to study the positive inotropic effect of amrinone in relation to the cyclic AMP and cyclic GMP metabolism. The positive inotropic effect of amrinone was accompanied by accumulation of cyclic AMP in the tissue: the cyclic AMP level was elevated in a similar time course to that of the increase in force of contraction and in a concentration-dependent manner in the presence of a beta adrenoceptor blocking agent, pindolol (3 X 10(-8) M). An excellent correlation was found between the force of contraction and cyclic AMP level in the presence of amrinone: the relationship was similar to that obtained previously with papaverine, a cyclic AMP phosphodiesterase inhibitor. The cyclic GMP level determined simultaneously was not changed by amrinone. The amrinone-induced increases in force of contraction and cyclic AMP level were markedly depressed by carbachol (3 X 10(-6) M); the relationship between the force of contraction and cyclic AMP level in the presence of amrinone was not changed by carbachol. Amrinone inhibited the cyclic AMP phosphodiesterase purified from the canine right ventricular muscle and enhanced the positive inotropic effect of isoproterenol. Amrinone shortened the time required for relaxation of a single contraction to the same extent as isoproterenol and cyclic AMP phosphodiesterase inhibitors such as 1-methyl-3-isobutylxanthine and papaverine. These results altogether strongly suggest that the change in cyclic AMP metabolism is involved in the positive inotropic effect of amrinone on the canine ventricular muscle.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1982

[Formation of secondary focus in amygdala Kindling phenomenon of the rabbit: a study by the coherence method].

Formation of the secondary focus in the rabbit amygdala Kindling (K) phenomenon was analysed by the coherence method. This method is capable of showing the degree of correlation between two signals (EEG) at each frequency. Mature male rabbits were used and a train stimulation using a biphasic square wave of 60 Hz was applied to the amygdala for two second once a day until the completion of K-phenomenon. The results obtained were as follows. 1) The coherence values between the amygdaloid K-region and opposite amygdala were usually much higher than those of the cerebral cortex (motor and optic areas) with a frequency of 6 to 7 Hz before and after completion of the K-phenomenon. 2) The speed of the secondary focus formation was observed to be parallel with the coherence value. 3) The secondary focus formation induced by the K of amygdala in a rabbit has much to do with the 6 Hz nerve circuit which links between the primary focus and secondary focus. That is, if the coherence value appears high around 6 Hz, the secondary focus is easily formed in case of a rabbit. 4) Application of this method enabled us to see the degree of functional correlation between the primary focus and secondary focus at each frequency. With all these, it is suggested that the theta frequency ranges of power spectra between above region play a vital role in producing secondary focus formation of the amygdaloid Kindling in rabbits.

Amygdala↗
PubMed1981

Effects of glyceryl trinitrate and SIN-1A on musculature and vasculature of the dog trachea in situ.

In dog trachea in situ, perfused arterially with blood, isoprenaline, glyceryl trinitrate and N-nitroso-N-morpholinoamino-acetonitrile (SIN-1A) given intra-arterially, decreased tracheal tone which had been elevated by neostigmine and increased tracheal blood flow. Glyceryl trinitrate and SIN-1A were more effective on the tracheal musculature than on the tracheal vasculature whereas isoprenaline was equally effective on both.

Aminoacetonitrile↗
PubMed1981

Effect of 2-nicotinamidethyl nitrate (SG-75) on membrane potentials of canine Purkinje fibers.

In canine Purkinje fibers firing spontaneously at a cycle length of about 2.7 sec, 2-nicotinamidethyl nitrate (SG-75) (10(-6)-10(-4)M) increased the cycle length and in high concentrations (10(-5)-10(-4)M) abolished the spontaneous firing. The increase in cycle length was due entirely to that decrease in slope of the diastolic depolarization which was more marked during late diastole than during early diastole. Neither the maximum diastolic potential nor the take-off potential was changed. When the membrane potential failed to reach the take-off potential, it polarized again after the early diastolic depolarization, in some fibers. The depth of the notch was increased and the peak value of the plateau of the action potential was decreased by SG-75, however, the maximum rate of rise of the action potential remained unchanged. Shortening of the action potential duration was evident when Purkinje fibers were stimulated at a cycle length of 2 sec. These fibers remained excitable at 10(-4) M SG-75 and when stimulated at a cycle length of 2 sec, the action potential occurred with a duration of less than half of control. These results can be interpreted as being due to an increase in the background K current induced by SG-75.

Animals↗
PubMed1981

Characterization of beta-adrenoceptors in the dog saphenous vein.

In vitro experiments were carried out on strips of the dog saphenous vein to characterize beta-adrenoceptors mediating relaxation. Four beta-adrenoceptor agonists, isoproterenol, salbutamol, procaterol and alpha-(3,4,5-trimethoxyphenethylaminomethyl)-3,4-dihydroxybenzylalcohol hydrochloride (T-1583), all produced concentration-dependent relaxation of venous strips contracted by 10(-6) M methoxamine. These four drugs behaved as full agonists. In producing venous relaxation, procaterol was about 2.5 times more potent, and salbutamol and T-1583 were 7 and 98 times less potent than isoproterenol, on a molar basis. The concentration-relaxation response curves to the four agonists were shifted in a parallel way to the right by (t-butyl-amino-3-ol-2-propyl)oximino-9 fluorene hydrochloride (IPS 339), a selective beta 2-adrenoceptor antagonist, and by practolol. However, pA2-values for IPS 339 against the four agonists were all nearly 11.0, whereas those for practolol were all nearly 5.7. We conclude that beta-adrenoceptors in the dog saphenous vein mediating relaxation are predominantly on the beta 2 type.

Adrenergic beta-Agonists↗
PubMed1981

Characterization of neuronal and vascular histamine receptors mediating the salivary and vasodilator responses to histamine of the dog submandibular gland.

The submandibular gland in situ was perfused with blood through the glandular artery at constant pressure in anesthetized dogs, and all drugs were administered intra-arterially. During infusion of metiamide, histamine and 2-(2-pyridyl)ethylamine (PEA) produced salivary and vasodilator responses consisting of an early and a late component. The dose-response curves for respective components of the salivary and vasodilator responses to PEA were parallel with the corresponding curves for histamine and in producing these responses PEA was about 40 times less potent than histamine on a molar basis. During infusion of mepyramine, histamine and dimaprit produced only the early vasodilator response. The dose-vasodilator response curves to histamine and dimaprit were parallel, and dimaprit was about 750 times less potent than histamine on a molar basis. The present results support the conclusion obtained in a previous study that neuronal histamine receptors mediating the whole salivary and the late vasodilator response are exclusively of the H1-type and vascular histamine receptors mediating the early vasodilator response consist of both H1-and H2-type although the former is predominant.

Animals↗
PubMed1981

Characterization of cardiovascular actions of CS-611, a new coronary dilator, in the dog.

In anesthetized, open-chest dogs 8-tert.-butyl-7,8-dihydro-5-methyl-6H-pyrrolo[3,2-e][1,2,4]triazolo[1,5-a]pyrimidine (CS-611), in doses of 0.1--1 mg/kg i.v. decreased systemic blood pressure, coronary resistance and arterio-venous O2 difference and increased coronary sinus outflow in a dose-related manner, but myocardial oxygen consumption was virtually unchanged. At 0.3 mg/kg i.v. of the drug, coronary sinus outflow was doubled, but heart rate and AV conduction time were not changed. In canine isolated, blood-perfused heart preparations, CS-611 only in large intra-arterial doses produced the following responses; a decrease in sinus rate followed by a slight increase in the SA node preparation, a transient prolongation of AV conduction time followed by a slight shortening in the AV node preparation and a transient decrease followed by a sizable increase in developed tension in the papillary muscle preparation. The drug in large intra-arterial doses decreased the rate of automaticity of the papillary muscle preparation. From these results CS-611 can be characterized as a coronary dilator virtually devoid of cardiac actions in doses sufficiently increasing coronary blood flow. By comparison of the present results with those of previous results on other coronary dilators it was revealed that CS-611 may have a novel mechanism of action.

Animals↗
PubMed1981

Effects of trapidil on musculature and vasculature of the dog trachea in situ.

In anesthetized dogs the trachea in situ was perfused with blood through the cannulated cranial thyroid arteries. The effects of trapidil on tracheal musculature and vasculature were assessed in comparison with those of isoproterenol and theophylline. All drugs were injected intra-arterially. Isoproterenol (0.03--0.3 microgram), trapidil (10--300 micrograms) and theophylline (30--300 micrograms) all produced an increase in tracheal blood flow (tracheal vasodilatation) and a decrease in the tracheal intraluminal pressure elevated by neostigmine (tracheal dilatation). In high doses the three drugs all produced maximal tracheal dilatation. Dose-response curves for tracheal vasodilatation to the three drugs were all parallel together, and trapidil was about 2700 time less potent than isoproterenol and about 3 times more potent than theophylline on a weight basis in producing tracheal vasodilatation. Dose-response curves for tracheal dilatation to the three drugs were also parallel together, and trapidil was about 880 times less potent than isoproterenol and about 3 times more potent than theophylline on a weight basis. When compared with isoproterenol, trapidil was about 3 times more effective on tracheal musculature than on tracheal vasculature, and theophylline resembled trapidil. The results suggest that trapidil can also be used as a bronchodilator.

Animals↗
PubMed1980

Dissociation of cyclic AMP and contractile responses to isoprenaline: effects of a dihydropyridine derivative, nicardipine (YC-93), on canine ventricular muscle.

Nicardipine (YC-93), a 1,4-dihydropyridine derivative, inhibited the cyclic AMP phosphodiesterase (PDE) activity of purified PDE in a cell-free preparation. Its inhibitory action on the purified PDE was about seven times that of papaverine. On the other hand, YC-93 did not affect the intracellular cyclic AMP level and the accumulation of cyclic AMP caused by isoprenaline in the isolated canine right ventricular myocardium. YC-93 caused a prominent negative inotropic action which developed gradually to reach a steady level 1 h after its administration. The potency of YC-93 to depress the force of contraction was one tenth that of D600. The dose-response curve for isoprenaline was shifted to the right and downward in the presence of YC-93 in a concentration-dependent manner, and the positive inotropic action of calcium was also inhibited markedly by YC-93. The depressant action of YC-93 on the positive inotropic actions of isoprenaline and calcium was more prominent than that of D600. Although YC-93 is a potent PDE inhibitor in the cell-free preparation, the PDE in the intact cell system may be not accessible to the drug. Thus, it is considered that YC-93 acted as a calcium antagonistic drug on the isolated canine ventricular myocardium, and thereby inhibited the positive inotropic action of isoprenaline without affecting the intracellular accumulation of cyclic AMP caused by isoprenaline.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1980

Coronary vasodilator and cardiac effects of optical isomers of verapamil in the dog.

Coronary vasodilator and cardiac effects of (-) and (+) verapamil were investigated in two kinds of canine heart preparations. When administered intravenously to anesthetized open-chest dogs, (-) verapamil was only 1.5-2 times as potent as (+) verapamil in increasing coronary sinus outflow and in decreasing mean arterial pressure and coronary resistance. However, (-) verapamil was about 5 times as potent in producing a negative chronotropic effect, about 10 times as potent in producing a negative dromotropic effect, and about 15 times as potent in decreasing myocardial oxygen consumption as (+) verapamil. When injected into the anterior septal artery in the isolated, blood-perfused papillary muscle preparation of the dog. (-) verapamil was about 15 times as potent as (+) verapamil in producing a negative inotropic effect. However, in increasing blood flow through the anterior septal artery (-) verapamil was only about 2.5 times as potent as (+) verapamil. These results indicate that in equieffective doses in producing coronary vasodilatation (+) verapamil is far less cardiodepressant than the (-) isomer.

Animals↗
PubMed1980

Differential effects of the calcium-antagonistic vasodilators, nifedipine and verapamil, on the tracheal musculature and vasculature of the dog.

In anaesthetized dogs the trachea in situ was perfused arterially with blood, and drugs were injected intraarterially. Isoprenaline and the calcium-antagonistic vasodilators, nifedipine and verapamil, increased tracheal blood flow and decreased resting tone of the trachea. Isoprenaline was equi-effective in producing tracheal vasodilatation and tracheal dilatation. The two calcium-antagonistic vasodilators were less effective tracheal dilators than tracheal vasodilators.

Animals↗
PubMed1980

Pharmacological analysis of salivary and blood flow responses to histamine of the submandibular gland of the dog.

1 The submandibular gland in situ was perfused with blood through the glandular artery at constant pressure in anaesthetized dogs. Drugs were administered intra-arterially. 2 Histamine produced both salivation and an increase in blood flow, each response having an early and a late component. 3 Marked tachyphylaxis to histamine developed in both of the salivary responses but only in the late blood flow response to histamine. 4 The early and late salivary responses were abolished and the late blood flow response was diminished by infusion of tetrodotoxin in doses that abolished the salivary and blood flow responses to electrical stimulation of the chorda-lingual nerve. 5 The whole salivary response to histamine was abolished by infusion of (--)-hyoscyamine in doses that greatly antagonized the salivary and blood flow responses to acetylcholine, whereas the blood flow responses to histamine were scarcely modified. These doses of (--)-hyoscyamine abolished the salivary response to chorda-lingual nerve stimulation but left the blood flow response to it unaffected. 6 The salivary and blood flow responses to histamine were unaffected by infusion of hexamethonium in doses that almost abolished the salivary and blood flow responses to chorda-lingual nerve stimulation. 7 The whole salivary response to histamine was abolished and the late blood response to histamine was partially inhibited by the histamine H1-receptor antagonist, mepyramine, but not by the histamine H2-receptor antagonist, metiamide. 8 The early blood flow response to histamine was antagonized by both mepyramine and metiamide but mepyramine was far more effective than metiamide. 9 These results led to the following conclusions: (1) the whole salivary response and a part of the late blood flow response to histamine are due entirely to excitation of parasympathetic postganglionic neurones; (2) neuronal histamine receptors involved are exclusively of the H1-type; (3) histamine has no direct stimulant action on the glandular cells; (4) the early blood flow response and the remaining part of the late blood flow response to histamine result from the direct action on vascular smooth muscle in the glandular vascular bed; (5) vascular histamine receptors consist of H1- and H2-receptors.

Animals↗
PubMed1980

Cholinergic intervention in intracardiac autonomic nerves in atrioventricular junctional area.

Cholinergic influence on atrioventricular (AV) junctional rhythm via its intervention in the intracardiac autonomic nerves was investigated in the canine, blood-perfused AV node preparation. Large amounts of acetylcholine (ACh) injected into the anterior septal artery (ASA) caused a rapid increase in the rate of automaticity superimposed on a slow increase. Nicotine given in the ASA caused to a rapid increased superimposed on a slow increase. Large amounts of ACh injected into the posterior septal artery (PSA) caused a slow increase, which was superimposed by a rapid icrease in the presence of l-hyoscyamine. The rapid and slow increases were abolished by dl-propranolol given in the PSA and ASA, respectively. Both types of increases were suppressed by tetrodotoxin (TTX). Nicotine given in the PSA caused a decrease superimposed by a rapid increase, both of which were abolished by TTX. These reslts indicate that cholinergic excitatory intervention induces AV junctional tachycardia via norepinephrine release from sympathetic nerve endings, distributing widely from the proximal to distal portion of the AV junctional area.

Acetylcholine↗