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Biomedical subjects

A Narimatsu

Publications and source records attributed to A Narimatsu.

68 records · Page 4Linked to original sources
PubMed1978

Effects on atrio-ventricular conduction of propranolol, pindolol and carteolol in the dog heart in situ as assessed by automated devices.

In open-chest dogs the heart rate was controlled at 150 beats/min and drugs were given intravenously. Propranolol (30 microgram/kg--1 mg/kg) prolonged the atrioventricular (A-V) conduction time and functional refractory period of the A-V conduction system (FRP) by blockade of the existing tone of the sympathetic nerves to the heart. The prolongation of the two parameters by the non-specific depressant action of propranolol was evident only at 3 mg/kg. Propranolol (3--30 microgram/kg) shortened the A-V conduction time in the heart deprived of the vagal and sympathetic tone, suggesting some sort of sympathomimetic effect. Pindolol in a wide range of doses (0.3--300 microgram/kg) exerted virtually no effect on the A-V conduction time and FRP, and its non-specific depressant action was apparent only at 3 mg/kg. Carteolol slightly prolonged the A-V conduction time and FRP only in low doses (1--10 microgram/kg), and in high doses (30 microgram/kg--1 mg/kg) it shortened the two parameters, reflecting its predominant sympathomimetic action.

Animals↗
PubMed1977

Positive dromotropic effect of dibutyryl cyclic adenosine 3',5'-monophosphate on the atrioventricular node.

The effect of atrioventricular (A-V) conduction of N6-2'-0-dibutyryl cyclic 3',5'-adenosine monophosphate (dibutyryl cyclic AMP) was investigated in comparison with those of norepinephrine, cyclic 3',5'-adenosine monophosphate (cyclic AMP), adenosine-5'-monophosphate (5'-AMP), and adenosine by the use of the isolated, blood-perfused A-V node preparation of the dog. Single injections of dibutyryl cyclic AMP (3-300 micronmol) and norepinephrine (0.1-1 nmol) into the posterior septal artery of the preparation (the upper part of the A-V node is mainly perfused through this artery) produced a dose-dependent decrease in the A-V conduction time. The time to the peak effect and the duration of the effect of dibutyryl cyclic AMP were much longer than with norepinephrine. The positive dromotropic effect of dibutyryl cyclic AMP was resistant to the beta-adrenoceptor blocking action of propranolol. Unlike dibutyryl cyclic AMP, cyclic AMP (above 30 nmol), 5'-AMP and adenosine (above 1 nmol) injected into the posterior septal artery prolonged the A-V conduction time in a dose-dependent manner. The results indicate that dibutyryl cyclic AMP has a mode of action on A-V nodal cells which differs distinctly from that of either norepinephrine or cyclic AMP, 5'-AMP, and adenosine.

Adenosine↗
PubMed1976

Effects of atrio-ventricular conduction of calcium-antagonistic coronary vasodilators, local anaesthetics and quinidine injected into the posterior and the anterior septal artery of the atrio-ventricular node preparation of the dog.

The effects on atrio-ventricular (A-V) conduction and blood flow of calcium-antagonists (verapamil, nifedipine and diltiazem), local anaesthetics (procaine and lidocaine) and quinidine were investigated in the isolated, cross-circulated A-V node preparation of the dog. The drugs were injected individually into the posterior septal artery (PSA) through which the upper part of the A-V node is mainly perfused or into the anterior septal artery (ASA) through which the lower part of the node and the more distal conduction system are perfused. Single injections into the PSA of nifedipine (0.3-10 mug), verapamil (1-30 mug), diltiazem (1-30 mug), quinidine (30-300 mug), lidocaine (100 mug-1 mg) and procaine (300 mug-3 mg) produced a dose-related increase in the A-V conduction time and with higher doses of these drugs a second or third degree block of A-V conduction occurred. Nifedipine (0.3-30 mug) and verapamil (1-100 mug) injected into the ASA scarcely affected A-V conduction. Quinidine (30 mug-1 mg) and lidocaine (100 mug-3 mg) injected into the ASA prolonged the A-V conduction time in a dose-related manner, although the effects were less prominent than those produced upon injection into the PSA. High doses of quinidine (3 mg) and lidocaine (3-10 mg) injected into the ASA altered the shape of ventricular bipolar electrograms and prolonged the time interval between an electrogram of the right bundle branch and that of the ventricle. The results are consistent with the hypothesis that in excitation of A-V nodal cells a slow calcium current rather than a fast sodium current plays an important role and that in the His-Purkinje-ventricular system the fast sodium current is predominant. Single injections of the 6 drugs into the PSA produced a dose-related increase in blood flow through the PSA. All drugs but nifedipine increased the blood flow in almost the same dose range that caused impairment of A-V conduction. Nifedipine was 10 times more potent in increasing the blood flow than in impairing A-V conduction.

Action Potentials↗
PubMed1975

Effects of nifedipine, a potent calcium-antagonistic coronary vasodilator, on atrioventricular conduction and blood flow in the isolated atrioventricular node preparation of the dog.

The effects of the calcium-antagonist nifedipine on atrioventricular (A-V) conduction and blood flow were investigated in comparison with those of verapamil by the use of the isolated, arterially blood-perfused A-V node preparation of the dog. Single injections of 0.3--30 mug of nifedipine and verapamil into the A-V node artery produced a dose-related increase in the A-V conduction time and at 30 mug the two drugs caused second degree block of A-V conduction. The results are compatible with the hypothesis that a slow calcium channel plays an important role in excitation of A-V nodal cells. The rate of blood flow through the A-V node artery was about 10 times more sensitive to nifedipine than was the A-V conduction time and increased in a dose-related manner. In contrast, an increase in blood flow rate by verapamil occurred in almost the same dose range as did impairment of A-V conduction. This indicates that the action of nifedipine is more pronounced on coronary smooth muscle cells than on the A-V nodal cells.

Animals↗
PubMedDate not supplied

Head and neck reconstruction with pectoralis major myocutaneous flap: CT evaluation.

Sixty-one CT scans in 20 patients who had undergone head and neck reconstructive surgery using a pectoralis major myocutaneous (PM-MC) flap were retrospectively evaluated to assess the usefulness of Ct in the follow-up of these patients. The normal CT findings in patients with PM-MC flaps are described. Of 13 cases with tumor recurrence, CT examination correctly detected recurrent masses in all cases, including 3 in which there was no clinical sign of recurrence. Postoperative masses mimicking tumor recurrence included deformed breast tissue, hematomas, lymphoceles, and abscesses. Computed tomography was of great value in the detection of tumor recurrence, but careful interpretation is required because a postoperative complication or anatomic alteration may lead to the erroneous diagnosis of tumor recurrence.

Abscess↗
PubMedDate not supplied

Anomalous left brachiocephalic vein: CT findings.

Eight cases of anomalous position of the left brachiocephalic vein were demonstrated by CT. Six coursed downward lateral to and below the aortic arch to enter the superior vena cava (SVC). Two cases were double left brachiocephalic veins. The superior branch was in the normal position, but the inferior vessel coursed below the aortic arch. Most of these subaortic left brachiocephalic veins enter the SVC at the same level or caudal to the azygous arch. Only two cases were associated with congenital heart disease. This anomalously positioned vessel is asymptomatic but must be distinguished from the pulmonary artery and persistent left SVC, especially when open heart surgery for cardiac malformations is being considered.

Adolescent↗
PubMedDate not supplied

Effects of antiarrhythmic drugs on AV nodal and intraventricular conduction as assessed in the isolated, blood-perfused AV node preparation of the dog.

The effects of seven antiarrhythmic drugs on atrioventricular (AV) nodal and intraventricular (His-Purkinje-ventricular muscle) conduction were investigated in the isolated, blood-perfused AV node preparation of the dog. When injected into the posterior septal artery (PSA), which supplies mainly the AV node, quinidine, ajmaline, disopyramide, lidocaine, mexiletine, phenytoin, and procainamide increased AV nodal conduction time; and in high doses, these drugs produced second- or third-degree AV conduction block. However, quinidine, ajmaline, disopyramide, and lidocaine had less propensity to induce second- or third-degree AV conduction block than did phenytoin, mexiletine, and procainamide. When injected into the anterior septal artery (ASA), which supplies the His-Purkinje-ventricular muscle, all seven drugs prolonged intraventricular conduction time. The relative suppressant effects of these drugs on AV nodal and intraventricular conduction varied. Quinidine, disopyramide, and ajmaline suppressed AV nodal conduction as much as intraventricular conduction. Lidocaine and mexiletine suppressed AV nodal conduction more than intraventricular conduction, and phenytoin suppressed AV nodal conduction much more than intraventricular conduction. In contrast, procainamide suppressed intraventricular conduction rather than AV nodal conduction. All drugs increased blood flow in the ASA and the PSA.

Animals↗
PubMedDate not supplied

Assessment of the coronary vasodilator action of SK&F 24260 in the dog.

1. The effects of SK&F 24260 administered intravenously or intraduodenally on the coronary outflow, coronary arteriovenous oxygen difference (A-V O2), myocardial oxygen consumption (MVO2), systemic blood pressure, heart rate and atrioventricular (AV) conduction time were examined in open-chest dogs. 2. SK&F 24260 in doses of 0.3-10 microgram/kg, i.v., caused a dose-dependent increase in coronary sinus outflow, but the increase was smaller with 30 microgram/kg, i.v., than with 10 microgram/kg, i.v. 3. SK&F 24260 (0.3-30 microgram/kg, i.v.) decreased A-V O2 and MVO2 in a dose-dependent manner. 4. SK&F 24260 (0.3-30 microgram/kg, i.v.) decreased systemic blood pressure and heart rate, and increased AV conduction time. 5. Intraduodenal administration of SK&F 24260 (1 mg/kg) produced almost the same effects on coronary sinus outflow, A-V O2, MVO2, systemic blood pressure, heart rate and AV conduction time as did the intravenous administration of the compound (10 microgram/kg). 6. The property of SK&F 24260 to increase the coronary blood flow and to moderately decrease MVO2, systemic blood pressure and heart rate indicates that this agent is a potential antianginal drug.

Animals↗