PubMed Health⌕ Search

Biomedical subjects

B Henning

Publications and source records attributed to B Henning.

32 records · Page 2Linked to original sources
PubMed1980

[Mexiletin for treatment of ventricular ectopic rhythm in patients with acute myocardial infarction (author's transl)].

In a controlled investigation on 84 patients with acute myocardial infarction, the effect of mexiletine on ectopic ventricular rhythms was tested with respect to mexiletine serum concentration. Malignant ventricular arrhythmias were observed 10 times in the control group and 5 times in the treated group. In the latter patients, mexiletine serum concentrations were below or at the lower therapeutical range (0.5 microgram/ml). During the second day of treatment, ventricular ectopic beats were significantly suppressed in the treated group with effective mexiletine serum concentration between 0.5 and 2.0 microgram/ml. As a side effect, vomiting was noticed in some patients in coincidence with an initial intravenous dosis of 2 mg per kg bodyweight; however, in no case it was necessary to interrupt treatment. There were no significant alterations in hemodynamical data, derived from Swan-Ganz catheter measurements, with mean maximal serum concentrations, on the second day, of approximately 1.15 microgram/ml.

Acute Disease↗
PubMed1979

[Ventricular arrhythmias in mitral valve prolapse syndrome (author's transl)].

Long-term ECG monitoring over 22 hours and exercise ECGs were performed in 72 patients with mitral valve prolapse syndrome. 70% of the patients had ventricular arrhythmias. In 28% severe arrhythmias in the form of multifocal atopic beats and ventricular runs were demonstrated. Long-term ECG monitoring was a suitable method for detection of these arrhythmias and superior to exercise ECG. Clinical, electrocardiographic and echocardiographic findings could not be correlated to the severity of ventricular arrhythmias.

Adolescent↗
PubMed1979

Circus movement in canine right ventricle.

The present study reports on the epicardial spread of excitation during premature beats and during the initial stages of ventricular fibrillation, both of which were induced by single-test stimuli during regional ischemia or local hypothermia. Simultaneous recording of the activity at 48 epicardial sites on the right ventricle of dog hearts enabled us in some instances to demonstrate a circus movement.

Animals↗
PubMedDate not supplied

Electrophysiological properties of human coronary endothelial cells.

The electrophysiological properties of human coronary endothelial cells (HCEC) of macro- and microvascular origin were studied using the whole-cell configuration of the patch-clamp technique. The membrane potential of confluent HCEC (-41.9 +/- 3.9 mV (mean +/- SEM, n = 32) for macro- and -33.6 +/- 2.6 mV (n = 64) for microvascular cells, respectively) was less negative than the K+ equilibrium potential. Inward currents of isolated cells at potentials below the K+ equilibrium potential were blocked by external Ba2+ (1 mM), inactivated due to time- and voltage-dependent block caused by external Na+, and their amplitudes were enhanced by increasing extracellular [K+]; these currents were identified as inwardly rectifying K+ currents. Some isolated cells displayed outwardly directed K+ currents which were abolished after replacement of Cs+ for K+ on both sides of the membrane. Voltage-dependent Ca2+ currents could not be observed in isolated HCEC. Hyperpolarizations induced by vasoactive agonists have been observed in some endothelial cells from different species. In contrast, extracellularly applied ATP (adenosine-5'-triphosphate) and ADP (adenosine-5'-diphosphate) at micromolar concentrations depolarized confluent HCEC, whereas adenosine had no effect on resting potentials (RP), indicating that the nucleotide-induced depolarizations were mediated via P2- purinoceptors. These depolarizations occurred even after replacement of N-methyl-D-glucamine for extracellular Na+, indicating that Ca(2+)-influx was involved. There were no marked differences in the electrophysiological properties between cells of macro and microvascular origin.

Adenosine Triphosphate↗
PubMedDate not supplied

Effect of tetrodotoxin, lidocaine, and quinidine on the transient inward current of sheep Purkinje fibres.

The effect of tetrodotoxin (TTX), lidocaine, and quinidine on the transient inward current (TI) was studied in voltage-clamped sheep cardiac Purkinje fibres. The TI was induced by elevation of extracellular Ca or addition of strophanthidin. Reduction of external Na had a biphasic effect on the steady state TI magnitude; a moderate (less than 50%) reduction of external Na had an enhancing effect on the TI; a further decrease of extracellular Na was accompanied by a decline of TI amplitude. The TI could not be induced in Na-free medium (external Ca less than or equal to 9.0 mM). TTX, lidocaine, and quinidine reduced the magnitude of the TI in a dose-dependent way. The blocking effect of these agents could be compensated for by a moderate (less than 50%) reduction of external Na or an elevation of extracellular Ca. It is suggested that the blocking effect of TTX, lidocaine, and quinidine on the TI is due to a reduction of intracellular Na, which causes a decay of intracellular Ca via the Na-Ca exchange mechanism.

Animals↗