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Biomedical subjects

K Obayashi

Publications and source records attributed to K Obayashi.

At least 73 records · Page 4Linked to original sources
PubMed1978

Electrophysiological effects of verapamil.

Previous studies have demonstrated that verapamil possess potent anti-arrhythmic effects. The present study has been designed to define the cardiovascular effects of this drug. Isolated tissue studies performed in rabbit right atrium demonstrated that prompt and prominent slowing of the sinus rate even at a dose of 1 X 10(-7) mol . litre-1. This dose produced significant decrease in action potential amplitude and phase 4 slope, shifted the 'threshold potential' to a less negative value, prolonged action potential duration but did not change maximum diastolic potential. At this dose of verapamil, sinoatrial conduction time prolonged significantly (control: 40.0 +/- 4.8 ms; 1 X 10(-7) mol . litre-1 verapamil: 50.0 +/- 6.4 ms). Purkinje fibre studies demonstrated decreases in dV/dt, resting potential, total amplitude, action potential duration at 75, 95% of recovery and effective refractory period only after exposure to greater than or equal to 1 X 10(-5) mol . litre-1 verapamil. Electrophysiological studies in conscious dogs demonstrated, after bolus administration of verapamil, progressive increases in the A-H interval and heart rate, but no changes in H-V and QRS intervals. Anaesthetised dog studies showed the lack of significant effect on A-H and H-V intervals or QRS duration regardless of the bolus dose of verapamil. However, verapamil produced statistically significant increases in heart rate after 0.025 mg . kg-1. Verapamil administration did not produce a statistically significant change in escape pacemaker rate in vagal stimulation experiments or with spontaneously beating isolated Purkinje fibres. Finally, the effect of increasing intravenous bolus does of verapamil on ischaemic arrhythmias was studied in five conscious dogs 24 h following LAD ligation. Only one dog with ventricular tachycardia and another dog with junctional escape rhythm were converted to sinus rhythm after the 0.05 mg . kg-1 and 0.2 mg . kg-1 doses, respectively. In conclusion, these studies demonstrated that administration of verapamil specifically depresses tissue with electrophysiological dependence on slow channel current. Therefore, sinus and A-V nodal events would be suppressed and slow-channel mediated events in ischaemic ventricle also would be inhibited. Clinically, acute administration of verapamil would lead to depression of sinus and A-V nodal function as well as potentially eliminate slow current mechanisms in ischaemic arrhythmias.

Animals↗
PubMed1976

Cardiovascular effects of ajmaline.

Ajmaline, a rauwolfia derivative, has been found to possess potent antiarrhythmic effects. The present study has been designed to define the cardiovascular effects of this drug. Hemodynamic studies performed in anesthetized and conscious dogs demonstrated no significant changes in measured hemodynamic parameters at doses equal to or less than 2 mg. per kilogram. Studies in isolated papillary muscle demonstrated no negative inotropic effects until concentrations of 1 X 10(-4). Disparate results were obtained with regard to heart rate reflecting the state of autonomic tone. Electrophysiologic studies in both anesthetized and conscious dogs demonstrated a significant depression of intraventricular conduction with no significant effect on AV nodal conduction; ventricular automaticity was not affected. Ajmaline did not alter digitalis-induced AV nodal conduction prolongation. However, ajmaline dramatically altered or abolished ventricular arrhythmias secondary to acute ischemia. In conclusion, these studies demonstrate that ajmaline specifically depresses intraventricular conduction, suggesting that this drug would be particularly effective in the treatment of re-entrant ventricular arrhythmias.

Ajmaline↗
PubMed1976

Electrophysiological effects of ajmaline in isolated cardiac tissue.

The electrophysiological effects of increasing molar concentrations of ajmaline were studied in isolated cardiac tissue, including sino-atrial node and Purkinje fibre. Ajmaline produced significant shortening of the plateau of Purkinje fibre action potential associated with marked depression of dV/dt and directly measured conduction velocity. A negative chronotropic effect was noted both in the sinus node and in spontaneously beating Purkinje fibres. Ajmaline's major electrophysiological effect appears to be depression of Purkinje fibre conduction velocity.

Action Potentials↗
PubMed1975

The Wolff-Parkinson-White syndrome: pharmacologic effects of procaine amide.

The effect of procaine amide, 10 mg. per kilogram via intravenous infusion, was studied in 13 patients with the WPW syndrome. The delta wave was eliminated by procaine amide in 10 and modified in three patients. This effect lasted between 30 minutes and 8 1/2 hours and was unrelated to the total dose administered. Anterograde A-V conduction was assessed by atrial pacing with increasing rates. More rapid atrial pacing rates with 1:1 A-V conduction were observed in patients who maintained rather than lost their delta wave during pacing. Ventriculoatrial conduction was assessed with ventricular pacing at increasing rates; ventricular conduction time was fixed regardless on the pacing rate. Procaine amide significantly prolonged V-A conduction time in six and blocked V-A conduction in one patient. In addition, A-V and V-A refractory periods were measured by the extrastimulus technique. Two types of responses were observed: (1) Type I or (2) line of identity. A-V nodal refractoriness was observed to be within the normal range. Procaine amide converted anterograde line of identity responses to Type I responses in all patients who had their delta waves eliminated. In this patient group, bypass refractoriness was shorter than A-V nodal refractoriness. Procaine amide was not observed to alter significantly normal A-V conduction as assessed by atrial pacing or A-V refractory period measurements. Furthermore, a significant disparity between the effects of procaine amide on anterograde and retrograde bypass refractoriness was observed. Tachycardias could be induced in nine of the 13 patients with a mean rate of 167.2 +/- 7.9 beats per minute; delta waves were abent during all episodes of tachycardia. Procaine amide prevented tachycardia induction in six of the none patients. Procaine amide therefore demonstrates electrophysiologic effects which would be beneficial for prevention or treatment of reciprocating tachycardias in the WPW syndrome. Moreover, procaine amide would be an ideal agent for the prevention of rapid ventricular rates in patients with the WPW syndrome and atrial fibrillation.

Adolescent↗
PubMed1975

Cardiorenal effects of lidocaine and procaine amide in the conscious dog.

Simultaneous measurements of hemodynamics, arterioventricular (AV) conduction, and renal functioner were obtained in conscious dogs. Catheters were implanted for the long-term measurement of central aortic, right ventricular, and pulmonary artery pressure. AV conduction was assessed following surgical implantation of multipolar electrode plaques in the area of the bundle of His, as well as on the epicardium of the right and left atria and ventricles. Renal function was assessed utilizing standard techniques. Following control measurements, lidocaine, 1 mg/kg, or procaine amide, 10 mg/kg, was administered intravenously. Subsequently, serial measurements were obtained for a 90-min period. No significant changes in hemodynamics were observed following either drug. Procaine amide produced a significant increase in heart rate and a minimal increase in QRS duration associated with a decrease in low right atrial to His bundle conduction time. However, no significant changes in cardiac conduction were observed after lidocaine administration. Renal function was unaffected by lidocaine but significantly depressed by procaine amide, as demonstrated by a decrease in GFR and effective renal flow. In summary, acute administration of procaine amide significantly alters renal function in the conscious dog with minimal effects on AV conduction and hemodynamics.

Aminohippuric Acids↗
PubMed1975

Atrioventricular nodal reentry in the Wolff-Parkinson-White syndrome.

Wolff, Parkinson, and White, in their initial description of the syndrome that bears their names, emphasized the association of tachycardias with the electrocardiographic abnormality. Subsequent investigations have identified, both anatomically and electrophysiologically, that dual pathways of atrioventricular (AV) conduction exist. Furthermore, experimental and clinical evidence has stressed that the mechanism of tachycardia production in the syndrome appears to reentry utilizing these dual pathways. However, recent studies have emphasized that other mechanisms of tachycardia production may be responsible for the arrhythmias seen in this syndrome. The present report identifies that AV nodal reentry may be the sole mechanism for tachycardia induction in the Wolff-Parkinson-White (WPW) syndrome. This finding may be of great clinical significance in light of the availability of surgical therapy for WPW patients with intractable arrhythmias.

Adolescent↗
PubMed1975

Prolongation of the tachycardia zone: a possible mechanism for medical failure in paroxysmal supraventricular tachycardia.

Paroxysmal supraventricular tachycardia in man has been considered to be due to either development of reentry utilizing AV junctional tissue or the presence of an ectopic pacemaker located within the atrium. Most contemporary information suggests that AV junctional reentry is the dominant mechanism for this arrhythmia in man. This present study identifies that the frequence of tachycardia episodes may be correlated with the width of a tachycardia zone as determined by the atrial extrastimulus technique. Moreover, pharmacological therapy directed toward the elimination of this arrhythmia can be assessed utilizing this atrial stimulation technique. Findings in this present study identify that, in patients with widened tachycardia zones, propranolol therapy may not be efficacious. This latter finding is no contrast to the previous observations suggesting that propranolol therapy is the drug of choice for reentrant arrhythmias in man.

Atrioventricular Node↗