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Biomedical subjects

T Beyer

Publications and source records attributed to T Beyer.

At least 55 records · Page 3Linked to original sources
PubMed1994

Effects of dihydropyridine calcium-antagonists on intracellular action potentials of rabbit sinus node, atrium and atrioventricular node. Comparison of felodipine with nifedipine.

The effects of the new dihydropyridine Ca-antagonist felodipine (CAS 72509-76-3) (3 x 10(-9) mol/l - 10(-6) mol/l) on intracellular action potentials of the rabbit sinus node and atrium were studied. Results were compared to the effects of nifedipine (10(-8) mol/l - 3 x (-10) mol/l). Additionally, rate-dependent effects of both substances on AV nodal conduction time were assessed. The data demonstrate a concentration-dependent reduction of sinus nodal automaticity due to depression of phase 4 automaticity concomitant with a reduction of the maximum upstroke velocity of the sinus action potential by both substances. Felodipine was about one half order of magnitude more potent than nifedipine. Both substances exerted little effects on action potentials in atrial cells. Felodipine and nifedipine led to a concentration and frequency-dependent ("use-dependent") retardation of AV nodal conduction. Again felodipine was about one half order of magnitude more potent than nifedipine.

Action Potentials↗
PubMed1993

Acute and chronic antiarrhythmic efficacy of d-sotalol in patients with sustained ventricular tachyarrhythmias.

To evaluate the clinical efficacy of d-sotalol, 84 patients with a history of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF), who had inducible sustained VT/VT at baseline electrophysiologic study (EPS), were investigated after intravenous (IV) d-sotalol (1.5-2.5 mg.kg-1). A total of 29 additional patients received only oral d-sotalol, (400-600 mg.day-1). Acute success of antiarrhythmic therapy was defined as suppression of inducible sustained VT/VF. The overall success rate of IV d-sotalol was 38% (32/84) after a mean of 4.3 drugs failed to suppress inducibility. A 78% success rate (31/40) was demonstrated in patients who were also assessed after oral d-sotalol. Torsade de pointes type VT was seen in one patient. After 1 year, only 16% of patients with a positive EPS had a recurrence compared to 43% of patients with a negative EPS (P < 0.05). Estimated survival rates were 95 and 88% after 1 and 2 years of follow-up, respectively. Only five of 56 patients discontinued d-sotalol therapy because of adverse effects. IV d-sotalol appears to be an effective antiarrhythmic agent. Its long-term efficacy is predictable on the basis of therapy guided by electrophysiologic testing in patients with refractory ventricular tachyarrhythmias. The efficacy of d-sotalol seems comparable to that reported for d,l-sotalol.

Cardiac Pacing, Artificial↗
PubMed1993

Comparative effects of d-sotalol and l-sotalol on the atrioventricular node of the rabbit heart.

The purpose of this study was to compare the dose-dependent effects of d-sotalol and l-sotalol (3 x 10(-7) M to 10(-4) M) on electrophysiological parameters in isolated preparations of the rabbit atrioventricular (AV) node. Standard microelectrode techniques were used in recording transmembrane action potentials from cells of the upper and lower AV node. Twelve New Zealand white Rabbits of either sex weighing between 1.5 and 2.6 kg were used. In both cell types studied, d-sotalol as well as l-sotalol prolonged action potential duration to the same extent. No significant effects were observed with either isomer on maximum diastolic potential, action potential amplitude, or maximum upstroke velocity of the action potential (Vmax). The rate of spontaneous discharge in AV nodal cells was decreased to the same extent by both isomers; this effect was caused by action potential prolongation; no effect on the rate of diastolic depolarization or Vmax was observed. Both d-sotalol and l-sotalol prolonged AV nodal conduction to the same degree by lengthening the action potential duration in AV nodal cells. The effects of 10(-4) M d-sotalol on AV nodal reentrant tachycardia were studied in one preparation in which AV nodal reentrant tachycardias could reproducibly be initiated by atrial premature stimulation. d-Sotalol abolished the occurrence of this tachycardia by lengthening refractoriness in AV nodal cells; this effect can be ascribed to a Class III antiarrhythmic effect.

Action Potentials↗
PubMed1993

[Ventricular tachyarrhythmia in acute and chronic myocardial ischemia: non-drug therapy and evaluation of outcome].

In recent years new methods of non-pharmacological therapy of ventricular tachyarrhythmias have gained increasing importance. The development of implantable defibrillators and increasing experience with catheter ablation techniques represent important alternatives to pharmacological antiarrhythmic therapy which is presently employed only in a subgroup of patients with life-threatening tachyarrhythmias and coronary heart disease.

Catheter Ablation↗
PubMed1992

Reduced adenylyl cyclase inhibition by carbachol and GTP during acute myocardial ischaemia.

Acute myocardial ischaemia frequently is complicated by ventricular tachyarrhythmias. These arrhythmias are in part due to an increased susceptibility of myocardial cells to adenylyl cyclase stimulation by catecholamines [1]. As adenylyl cyclase underlies an endogenous dual regulation by stimulatory and inhibitory receptor systems, adenylyl cyclase stimulation can be counteracted by the activation of receptors like the muscarinic M2 receptor [2]. Therefore, the effect of myocardial ischaemia on muscarinic receptor and "inhibitory" guanine nucleotide binding proteins (G(i)) mediated inhibition of adenylyl cyclase was studied. During 5 min of myocardial ischaemia, carbachol mediated inhibition of forskolin and isoproterenol stimulated adenylyl cyclase was reduced by 30% and 50%, respectively. Hormone independent inhibition of adenylyl cyclase by the nonhydrolyzable GTP-analogue guanosine 5'-[beta gamma-imido]triphosphate (Gpp(NH)p) was reduced by 46%. In contrast, the amount of G(i), as determined by pertussis toxin catalyzed ADP-ribosylation, remained constant during 15 min of ischaemia. The impaired function of muscarinic receptor linked signal transduction during early myocardial ischaemia could contribute to the occurrence of ischaemia induced tachyarrhythmias by a reduced ability to counteract adenylyl cyclase activation.

Adenylyl Cyclase Inhibitors↗
PubMed1992

The effects of neuroleptics on facial action in schizophrenic patients.

This paper describes the influence of neuroleptic therapy on facial action in drug-naive schizophrenics. In a comparative study of medicated and unmedicated schizophrenic patients, the coordinates of 12 small light-reflecting points, attached to subjects' faces, were computer-recorded and analyzed automatically during a semi-standardized clinical interview. In addition, facial activity in videotaped interviews was coded using the Facial Action Coding System (FACS). Each sample group comprised of eight patients with the DSM-III-R diagnostic criteria "schizophrenia" or "schizophreniform disorder". Subjects were studied on two occasions, one shortly after admission to the hospital, the other three weeks later. Group 1 was unmedicated during the first session, whereas group 2 was medicated throughout the study. Three weeks after the start of medication, at the second interview, both recording methods showed a reduction in facial activity and facial expression across all subjects in group 1. The facial action of patients in group 2, however, remained unchanged.

Adult↗
PubMed1992

Sotalol exhibits reverse use-dependent action on monophasic action potentials in normal but not in infarcted canine ventricular myocardium.

In 12 anesthetized mongrel dogs (30 mg/kg pentobarbital), a thoracotomy was performed, and the left anterior descending coronary artery was ligated proximally. Eight to 12 days later, monophasic action potentials were recorded endocardially from the apex of the noninfarcted right ventricle and infarcted areas of the left ventricle, and the effects of 1.5 mg/kg intravenous sotalol were evaluated. Monophasic action potentials from the infarcted zone of the left ventricle were obtained from areas where fractionated bipolar electrograms could be recorded; this was histologically confirmed. After sotalol, in sinus rhythm, the monophasic action potential duration at 90% repolarization of the infarcted zone increased from 186 +/- 31 to 226 +/- 45 ms (+ 22%, p less than 0.05), and monophasic action potential duration of the noninfarcted zone increased from 184 +/- 31 to 225 +/- 47 ms (+ 22%, p less than 0.05). Programmed ventricular stimulation was performed with single extrastimuli at a basic drive cycle length of 300 ms. With long coupling intervals (290 ms), monophasic action potential duration of the infarcted zone increased from 165 +/- 23 to 183 +/- 25 ms (+ 11%, p less than 0.05) after sotalol; and monophasic action potential duration of the noninfarcted zone increased from 159 +/- 20 to 180 +/- 25 ms (+ 13%, p less than 0.05). With short coupling intervals (200 ms), the monophasic action potential duration of the noninfarcted zone increased from 157 +/- 19 to 173 +/- 18 ms (+ 10%, p less than 0.05), and monophasic action potential duration of the noninfarcted zone increased from 150 +/- 18 to 157 +/- 18 ms (+ 5%, NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1992

Differential effects of quinidine on transmembrane action potentials of normal and infarcted canine Purkinje fibers.

Fourteen days after proximal ligation of the left anterior descending coronary artery (LAD) of mongrel dogs, the effects of quinidine on action potentials of normal and infarcted Purkinje fibers were evaluated. The concentration-dependent (10(-7)-3 x 10(-5) M) and frequency-dependent (1 and 3 Hz) actions of quinidine were evaluated by the following parameters: maximum upstroke velocity (Vmax), action potential duration at 50 and 95% repolarization (APD50, APD95), effective refractory period (ERP), resting membrane potential (RMP), and action potential amplitude (APA). Quinidine reduced Vmax in normal and abnormal Purkinje fibers in a concentration- and frequency-dependent manner; these effects were more pronounced in infarcted tissue. The APD50 was shortened significantly at 1 Hz in noninfarcted Purkinje fibers, whereas in infarcted Purkinje fibers quinidine had no effect on APD50. The APD95 was not significantly altered by quinidine in normal Purkinje fibers; in infarcted areas APD95 was significantly prolonged at 1 and 3 Hz. The effective refractory period (ERP) was prolonged in normal and infarcted Purkinje fibers, these effects were more marked in ischemically damaged fibers. No effects were observed on resting membrane potential (RMP). APA was reduced significantly after quinidine at 1 and 3 Hz; there was no difference between normal and infarcted tissue. These data indicate a differential effect of quinidine in normal and infarcted Purkinje fibers which may be an important mechanism of action of quinidine in infarcted tissue.

Action Potentials↗
PubMed1992

Electrophysiologic and antiarrhythmic effects of D-sotalol.

There is extensive experimental and clinical experience concerning the antiarrhythmic potency of DL-sotalol, a beta-adrenergic antagonist that lengthens the cardiac action potential duration. More recently, its dextrorotatory isomer, D-sotalol, has been evaluated in experimental studies and preliminary clinical trials. Whereas the isomer is almost free of beta-blocking activity, both experimental and clinical data demonstrate that potent class III activity of D-sotalol. Further investigations, particularly in patients with life-threatening arrhythmias, are needed to delineate the clinical usefulness of this compound.

Action Potentials↗
PubMed1991

Reverse use-dependent effects of sotalol demonstrated by recording monophasic action potentials of the right ventricle.

In 22 patients referred for electrophysiologic study, monophasic action potentials (MAP) were recorded from the right ventricular aspect of the ventricular septum. The duration of MAP at 90% (MAP90) and 30% (MAP30) repolarization was measured in sinus rhythm, at a constant atrial paced cycle length of 600 ms for 3 minutes and at constant ventricular paced cycle lengths of 600, 500, 400 and 300 ms for 20 beats. Programmed ventricular stimulation from the apex of the right ventricle was performed at a basic drive cycle length of 400 ms and MAP90 and MAP30 of premature beats was determined. Changes of MAP duration were assessed 20 minutes after administration of intravenous sotalol 1.5 mg/kg. Sotalol significantly increased MAP90 and MAP30 in sinus rhythm. This was independent from sinus cycle length prolongation as evidenced by a significant prolongation of MAP90 and MAP30 with constant atrial pacing after sotalol. With slow ventricular stimulation frequencies and with long coupling intervals at programmed ventricular stimulation, sotalol significantly prolonged MAP90 and MAP30; with high stimulation frequencies and at short coupling intervals the action potential-prolonging effect of sotalol was diminished, indicating a reverse use-dependent effect of sotalol on repolarization of the right ventricle in humans.

Action Potentials↗
PubMed1991

Characteristics of endocardial monophasic action potentials recorded from areas with fractionated bipolar electrograms in infarcted canine ventricular myocardium.

STUDY OBJECTIVE: The aim was to characterise monophasic action potentials recorded from subacutely infarcted myocardial regions, where fractionated bipolar electrograms could be obtained. DESIGN: Dogs underwent ligation of the left anterior descending coronary artery. Before and 8-12 d after ligation, monophasic action potentials and local electrograms were recorded endocardially from the apex of the left ventricle. EXPERIMENTAL MATERIAL: 15 anaesthetised mongrel dogs (30 mg pentobarbitone.kg-1) were used. MEASUREMENTS AND MAIN RESULTS: Multiphasic fractionated bipolar electrograms could be recorded from infarcted sites of the left ventricle with a mean duration of 69(SD 10) ms and a mean amplitude of 3.7(1.6) mV, compared to control values of 42(7) ms (p less than 0.05) and 9.4(2.2) mV (p less than 0.05), respectively. Endocardial monophasic action potentials recorded from these areas were similar to action potentials obtained from non-infarcted sites before coronary ligation. The fractionated extracellular potentials were superimposed on the monophasic action potential upstroke. MAP90 was 189(31) ms, MAP30 138(12) ms, versus control values of 182(27) ms and 139(10) ms (NS). Monophasic action potential amplitude was significantly reduced at infarcted sites compared to control, at 26(7) mV v 38(6) mV. Histological specimens were taken to confirm that measurements were obtained from infarcted tissue. CONCLUSIONS: It is possible to record monophasic action potential in subacutely infarcted canine ventricular myocardium; this technique might help in further studies to characterise electrophysiological mechanisms of ventricular arrhythmias in chronic myocardial infarction in man.

Action Potentials↗
PubMed1991

Distribution and DNA methylation of a repetitive promoter sequence cloned from mouse embryonal carcinoma cells.

A 203 bp HpaII fragment (X9) cloned from F9 embryonal carcinoma cell DNA showed multiple bands on Southern hybridization towards mouse DNA digested with various restriction enzymes. No tandem repeats were evident. A 200 bp MspI band corresponded to several copies of the cloned fragment and many elements appeared each associated with a 12-kb PvuII fragment. X9 is therefore a member of a moderately repetitive family probably dispersed in the mouse genome. X9 displayed polymorphisms between different Mus species, whereas multiple hybridizing bands were detected neither in DNA from rodent species outside the Mus genus nor in DNA from man. Therefore, X9 provides a useful probe for studies of murine evolution. X9 contains a TATA box and a CCAAT box as well as several homologies to known transcription factor binding sites. When cloned in front of a reporter gene, it acted as a strong promoter in several different cell types. Most genomic sequences detected by X9 were highly methylated. A single copy appeared hypomethylated in adult mouse tissues, whereas several copies were hypomethylated in F9 and embryonic stem cells. It is speculated that X9 might represent the promoter of a murine gene family whose activity is regulated by DNA methylation.

Animals↗
PubMed1991

[Combined anti-bradycardia/anti-tachycardia pacemaker-cardioverter-defibrillator systems in patients with recurrent ventricular tachyarrhythmias].

In 41 patients with recurrent sustained ventricular tachycardia and/or ventricular fibrillation an integrated pacemaker-defibrillator-system (PCD, Medtronic, model 7216 A or 7217 B) was implanted. In 21 out of 24 (88%) patients a new transvenous implantation technique in combination with a subcutaneous patch electrode was used. The implanted devices comprise antibradycardiac pacemaker functions, two different forms of antitachycardiac pacemaker functions (ramp and burst pacing), and internal cardioversion or defibrillation capabilities. During a mean follow-up of 8 months 147 episodes of ventricular tachycardia were detected, 131 of them were terminated successfully by antitachycardiac pacing; in 13 episodes internal cardioversion was applied to revert ventricular tachycardia. Twenty-seven episodes of ventricular fibrillation or rapid ventricular tachycardia (greater than 200/min) were detected and successfully terminated by internal defibrillation. In six patients with intermittent rapid atrial fibrillation, change of antiarrhythmic therapy was required to avoid activation of the device. The new integrated pacemaker-defibrillator systems improve therapy in patients with life-threatening tachyarrhythmias by reducing the number of internal cardioversions/defibrillations; the non-thoracotomy approach reduces the post operative risk.

Adult↗
PubMed1990

Electrophysiologic effects of bepridil in patients with refractory ventricular tachycardia assessed by programmed electrical stimulation.

The effect of intravenous bepridil, a new calcium antagonist with class I and III properties, was tested in 21 patients with sustained ventricular tachyarrhythmias refractory to a mean of five antiarrhythmic agents as assessed by programmed right ventricular stimulation. At control electrophysiologic study without antiarrhythmic agents, sustained monomorphic ventricular tachycardia (VT) was initiated in 20 patients and ventricular fibrillation (VF) was initiated in one patient. After 3 mg/kg of bepridil was administered, VT was still inducible in 19 patients (3 patients had self-terminating VT); the other 2 patients had no inducible VT after bepridil. Bepridil prolonged significantly the QTc interval, the effective refractory period, and the cycle length of induced ventricular tachycardia. Two patients with no inducible VT after intravenous bepridil were placed on oral bepridil (300 mg/day). One patient died suddenly and one patient died of progressive heart failure. The results seem to indicate that the efficacy of bepridil in patients with refractory ventricular tachycardia is limited.

Aged↗
PubMed1989

[Proarrhythmic effect of ajmaline in idiopathic ventricular tachycardia].

A 23-year-old woman was hospitalized because of life-threatening monomorphic ventricular tachycardia (VT) of 150 beats/min. An intravenous bolus of lidocaine was without effect but 25 mg ajmaline converted the tachycardia to sinus rhythm. A total of 70 mg ajmaline was subsequently infused because of frequent ventricular premature systoles. During this treatment polymorphic VT with very wide QRS complexes developed, but spontaneously disappeared after ajmaline had been discontinued. The case demonstrates the need for taking into account the potential risk of a proarrhythmic effect of anti-arrhythmic drugs.

Adult↗