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Biomedical subjects

J Senges

Publications and source records attributed to J Senges.

At least 163 records · Page 9Linked to original sources
PubMed1982

Arrhythmogenic effects of toxic concentrations of the antiarrhythmic drug lorcainide on the isolated canine ventricle.

The effect of the new antiarrhythmic drug lorcainide was studied on the specialized conducting system of isolated canine ventricle. Transmembrane action potentials were recorded simultaneously from three subendocardial sites within the ventricular basis, free wall and apex. At concentrations of 3 x 10(-6) and 2.4 x 10(-5) M, lorcainide caused a dose-dependent decrease in maximum rates of rise and in amplitude of the action potential; 0.6 x 10(-6) M had no significant effect, resting potential and action potential duration remained unchanged with 0.6 x 10(-6) M and 3 x 10(-6) M. The most prominent effect of 2.4 x 10(-6) M lorcainide was the appearance of an increasing notch resulting in clear separation of the action potential in an initial short spike depolarization (50-120 msec) with or without a subsequent plateau depolarization 280-370 msec). Both components demonstrated an independent and inhomogeneous conduction through functionally different pathways. Changes in stimulation rate or premature stimuli resulted in nonstimulated reexcitations resembling bigemini, ventricular tachycardia or regional ventricular fibrillation. The results indicate that dissociation of the action potential in two components is due to toxic alterations of ionic channels of the fiber membrane and that nonstimulated reexcitations are due to reentry via functionally fast and slow pathways.

Action Potentials↗
PubMed1981

[Direct contrast medium demonstration of acute and chronic pericardial effusion and of the pericardium (author's transl)].

After aspiration of the pericardial space 10 to 20 ml of contrast medium were injected into the pericardial sac in 11 patients with in part large pericardial effusions. Thus the effusion became directly visible on fluoroscopy and a satisfactory position of the aspiration cannula in the pericardial sac was ascertained. Complete drainage of the pericardial effusion could be well observed by fluoroscopy. The pericardial effusion dyed by contrast medium and the surrounding structures could be filmed by kinecardiography with a 35 mm camera ("pericardiography"). In contrast to echocardiography pericardiography resulted in additional important diagnostic information in two patients. Direct contrast medium demonstration of pericardial effusions and of the pericardium improves the safety during pericardial aspiration and enlarges the diagnostic possibilities particularly in ill-defined pericardial diseases and septated pericardial processes.

Adult↗
PubMed1981

[Effect of intracoronary fibrinolysis on left ventricular diastolic function in patients with acute myocardial infarction (author's transl)].

In 22 patients with acute myocardial infarction, intracoronary infusion of streptokinase was begun 3.2 +/- 1.4 hours after the onset of symptoms. In 71% of patients recanalization of a completely occluded artery could be achieved. In 12 successfully treated patients left ventricular hemodynamics (left ventricular diastolic compliance and regional wall motion) were compared before and 4 weeks after recanalization. 4 weeks after intracoronary fibrinolysis left ventricular end-diastolic pressure had fallen (from 20 to 15 mm Hg, p less than 0.05), diastolic compliance had improved (p less than 0.05) and infarct size was reduced (p less than 0.05) compared to the acute stage of myocardial infarction. Left ventricular hemodynamics of 16 patients without heart disease (group A) and 22 patients with chronic myocardial infarction treated medically (group B) were compared to the findings of patients with acute myocardial infarction (group C). Group B and C showed reduced diastolic compliance as compared to group A (p less than 0.001). When group B and c were compared with identical size of akinesis (as measured by the number of asynergic hemiaxes), there was no significant difference of diastolic compliance. Reduction of diastolic compliance correlated linearly with infarct size (r = 0.73, r = 0.78). The results indicate that successful early reperfusion of acute myocardial infarction leads to a reduction of infarct size.

Adult↗
PubMed1979

Effect of hypoxia on the sinoatrial node, atrium, and atrioventricular node in the rabbit heart.

We used intracellular microelectrodes to study the effects of hypoxia on the isolated, superfused sinoatrial (SA) node, atrium, and atrioventricular (AV) node of the rabbit heart. Hypoxia decreased the rate of spontaneous impulse initiation in SA nodal fibers by decreasing the slope of diastolic depolarization. With gradually decreasing Po2, the sinus rate was reduced; concomitantly, the corrected sinus node recovery time after rapid atrial stimulation was much less affected demonstrating marked prolongation only under severe anoxic conditions. Hypoxia decreased the amplitude of action potentials of the SA node and of the AV node but not of the atrium. SA and AV nodal conduction were slowed by hypoxia; intraatrial conduction was not significantly affected. AV nodal conduction block occurred at lower atrial rates, and the effective refractory period of the AV node was prolonged. Inhomogeneity of SA and AV nodal impulse propagation often was observed in the presence of hypoxia. This was associated with concealed reentry within both nodal areas. The extracellular K+ concentration of the atrial tissue was measured with ion-sensitive microelectrodes. [K+]o remained unchanged even after prolonged periods of severe hypoxia. These results are consistent with the hypothesis that acute hypoxia predominantly inhibits slow response activity but has only little effect on the fast inward sodium current.

Action Potentials↗
PubMed1979

Effects of some components of ischemia on electrical activity and reentry in the canine ventricular conducting system.

We used intracellular microelectrodes to study the electrophysiological effects of combinations of components of ischemia and their relation to the occurrence of ventricular arrhythmias in the specialized conducting system of isolated canine right ventricles. The middle area of the free wall was exposed to various test solutions in the center compartment of a three-chambered bath; the base and apex of the preparation were superfused with normal Tyrode's solution in the outer control compartments. Hypoxia (Po2 40 mm Hg), lactic acidosis (pH 6.5), and orciprenaline (10(-6) M), either alone or combined, failed to affect the action potential amplitude or the conduction velocity of the subendocardial fibers, and no arrhythmias occurred. The action potential duration and the effective refractory period were markedly prolonged by lactic acidosis. Exposure of the test regions to 15 mM K+ plus orciprenaline resulted in marked decreases in action potential amplitude and conduction velocity. Abnormalities of impulse transmission through the depressed area included high degrees of rate-dependent block, one-way block, warming-up phenomenon, and the Wenckebach phenomenon. Such conditions regularly provoked the appearance of single, sustained, or concealed reentrant depolarizations. The combined effects of hypoxia, 15 mM K+, and orciprenaline resulted in further depression of the already depressed action potential in the depolarized fibers. Our results indicate that regional increases of extracellular K+ may be the predominant factor of the components of ischemia we studied which facilitates the initiation of reentrant arrhythmias.

Acidosis↗
PubMed1979

Nitrates and ectopic ventricular activity in mitral valve prolapse: clinical and experimental data.

Three patients with mitral valve prolapse, high grade ventricular arrhythmias and a strong family history of sudden death were studied utilizing continuous Ecg monitoring and intracardiac stimulation and recording techniques. Analysis of 6-hour ambulatory Ecgs revealed frequent premature ventricular beats (PVBs) including repetitive and multiform PVBs in each patient. The electrophysiological studies demonstrated normal parameters of intracardiac conduction and refractoriness providing no evidence for reentrant mechanisms. Acute drug testing with 0.4 mg sublingual nitroglycerin completely suppressed all ventricular arrhythmias. During maintenance therapy antiarrhythmic nitrate efficacy was only partly confirmed monitoring the effects of 4 x20 mg isosorbide dinitrate on 6-hour ambulatory Ecgs. The electrophysiological parameters of intracardiac conduction and refractoriness were not significantly altered by 0.4 mg sublingual nitroglycerin. Experimental data obtained from isolated rabbit atria and canine ventricles revealed no significant action of nitroglycerin in the parameters of cardiac automaticity and conduction including transmembrane electrical activity of normal and hypoxically damaged SA nodal, atrial and ventricular fibers. It is concluded that a) PVBs in patients with mitral prolapse appear related to ectopic automaticity; b)nitrates may suppress ventricular ectopy in these patients; c) antiarrhythmic nitrate efficacy is not related to direct membrane effects.

Animals↗
PubMed1977

Ventricular arrhythmias in cardiac anaphylaxis.

Arrhythmogenic effects of anaphylaxis and histamine were studied in guinea pigs by measuring changes of transmembrane potentials from isolated papillary muscles. Antigenic challenge of preparations obtained from passively sensitized animals induced ventricular automaticity in 1/3 of the experiments. The arrhythmogenic effects of cardiac anaphylaxis could be reproduced by exogenous histamine. Abnormal automaticity was associated with a stable diastolic membrane potential in most of the ventricular fibres and only occasionally ectopic pacemaker potentials were observed in fibres near the ventricular septum. The effective refractory period, maximum rate of depolarization of the action potential and electrical threshold were not significantly changed in ventricular anaphylaxis but in the presence of histamine the refractory time was shortened. Ventricular arrhythmias induced by histamine were increased at high extracellular Ca2+ concentrations and inhibited by Mn2+ and D 600 but were only moderately antagonized by tetrodotoxin. Pretreatment with reserpine had no effect on the abnormal automaticity. Spontaneous ventricular activity caused by histamine was markedly inhibited by the histamine H2-receptor antagonist burimamide and also by the antiarrhythmic drug, prajmalium bitartrate. The H1-receptor antagonist brompheniramine, hydrocortisone and propranolol had little or no antiarrhythmic effect.

Action Potentials↗