Biomedical subjects

Y Ogiwara

Publications and source records attributed to Y Ogiwara.

40 records · Page 3Linked to original sources

PubMedDate not supplied

Effects of ketanserin on the pacemaker activity and contractility in the isolated, blood-perfused dog atrium.

Effects of ketanserin on the pacemaker activity and atrial contractility and on 5-hydroxytryptamine (5-HT)-induced cardiac responses were investigated in the isolated, blood-perfused dog atrium. Ketanserin (1-300 micrograms) injected into the sinus node artery evoked a transient positive followed by a negative chronotropic effect, and a dose above 30 micrograms of ketanserin produced a dose-dependent negative inotropic effect with a little positive one. Ketanserin-induced negative chronotropic and inotropic effects were not affected by atropine in a dose which blocked ACh-induced responses. Propranolol inhibited positive inotropic responses to ketanserin and norepinephrine and significantly augmented the negative chronotropic and inotropic responses to ketanserin. Imipramine did not affect the transient positive followed by negative chronotropic and the negative inotropic responses to ketanserin but it induced the positive cardiac responses following the negative ones. Tetrodotoxin, phentolamine, and diphenhydramine did not modify the effects of ketanserin. From these results, it is concluded that ketanserin might induce the direct negative chronotropic and inotropic effects and the indirect effects by catecholamine release. Ketanserin-induced catecholamine release might not be due to tyramine-like or nicotine-like action. Ketanserin significantly inhibited a low dose (3 micrograms) of 5-HT-induced negative chronotropic and inotropic effects, suggesting the possibility of 5-HT2 receptors in the isolated dog atrium.

Animals↗

PubMedDate not supplied

Positive chronotropic and inotropic effects of pimobendan (UD-CG 115 BS) in isolated, cross-circulated canine heart preparations.

The effects of pimobendan on the sinus node pacemaker activity and atrial contractility and on the left ventricular contractility were investigated in the isolated, cross-circulated right atrial and left ventricular preparations of the dog. Pimobendan, at a dose range of 1 to 1,000 nmol, injected into the sinus node artery of the isolated atrium, induced dose-dependent positive inotropic and chronotropic responses. At the same doses, it also induced dose-dependent increases in the left ventricular contractile force, similar to those in the atrial one, although the norepinephrine (NE)- and isoproterenol-induced positive inotropic effects in the ventricles were less than those in the atria. The positive cardiac effects were not inhibited by propranolol but they were depressed by intramural vagal nerve stimulation. These results suggest that pimobendan increases left ventricular contractility more effectively than atrial contractility in comparison with a beta-adrenoceptor agonist and that the positive cardiac effects of pimobendan were partially induced by a phosphodiesterase inhibition but not by a beta-adrenoceptor activation in the dog heart. When pimobendan, at a dose of 10 to 1,000 micrograms/kg, was cumulatively administered into the jugular vein of the support dog, a decrease in arterial blood pressure and an increase in heart rate were dose-dependently observed in the support dog. Half a minute after administration, the positive inotropic and chronotropic responses were induced in the isolated atrium in a dose-related manner. The pimobendan-induced positive cardiac effects were not inhibited by i.v. administration of propranolol, whereas the isosorbide dinitrate-induced positive chronotropic effects were significantly inhibited. These results indicate that pimobendan directly increases cardiac contractility and heart rate with vasodilatation in anesthetized dogs.

Adrenergic beta-Antagonists↗

PubMedDate not supplied

Effects on atrio-ventricular conduction of alinidine and falipamil injected into the AV node artery of the anesthetized dog.

The effects of the bradycardic agents alinidine and falipamil, on atrio-ventricular (AV) conduction were compared with those of other negative chronotropic agents, acetylcholine (ACh), carbachol (CCh), adenosine and verapamil, in open-chest, anesthetized dogs. When each drug was selectively administered into the AV node artery, none of them changed the sinus rate and arterial blood pressure. Although alinidine did not significantly change the atrio-ventricular conduction time (AVCT), falipamil and others induced a dose-dependent prolongation of the AVCT. The order of the AVCT prolongation was CCh greater than ACh greater than verapamil much greater than adenosine greater than falipamil much greater than alinidine. ACh, CCh and verapamil frequently caused second or third degree AV block at higher doses. The His bundle electrocardiogram revealed that all AV blocks occurred between the atrium and the His bundle (A-H block). The CCh-induced prolongation of the AVCT, but not the adenosine-induced prolongation, was significantly suppressed by treatment with alinidine or falipamil. These results indicate that alinidine scarcely affects AV conduction in the in situ dog heart and that the muscarinic cholinergic receptor blocking effect of alinidine or falipamil modifies the AVCT secondarily when vagal activity is maintained.

Anesthesia↗

PubMedDate not supplied

Bradycardic effect of alinidine on in situ and on isolated, blood-perfused heart preparations of dogs.

The cardiovascular effects of alinidine were studied on the donor dog and on the isolated dog right atrial or left ventricular preparation which was cross-perfused with arterial blood from the donor dog. When heart rate and systemic arterial blood pressure of the donor dog were decreased dose-dependently by i.v. administration of alinidine (10-300 micrograms/kg), decreases in atrial rate and atrial developed tension of the isolated preparation were induced in a dose-dependent manner, confirming that i.v. administration of alinidine directly induced negative chronotropic and inotropic effects in situ dog heart. The negative chronotropic effects at lower doses of alinidine were more prominent than the decrease in blood pressure of the anesthetized dog and the negative inotropic effect of the isolated atrium, respectively. Direct injection of alinidine (1-300 micrograms) into the sinus node artery of the isolated atrium induced predominant negative chronotropic responses at lower doses. In paced left ventricular muscle preparations, alinidine reduced the developed tension at higher doses. Ratios (decreases in atrial developed tension per decreases in atrial rate) for alinidine ranged from 1.2 to 2.1, which were smaller than those of acetylcholine, adenosine and verapamil, suggesting that alinidine has a predominant bradycardic property and induces bradycardia due to a different mechanism from those of other bradycardic agents in the isolated and blood-perfused dog heart. The responses to isoproterenol and norepinephrine were suppressed significantly by treatment with alinidine (300 micrograms) predominantly on chronotropism. The alinidine-induced decreases in atrial rate were relatively greater when the rate had been augmented by dibutyryl cyclic AMP and norepinephrine infusion, but the relative depression of contractility was slight. From these results, it is suggested that alinidine attenuates the positive chronotropic effects induced by increases in cyclic AMP without decreasing the positive inotropic ones in the blood-perfused dog atrium.

Animals↗