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Biomedical subjects

H Heuer

Publications and source records attributed to H Heuer.

118 records · Page 7Linked to original sources
PubMed1982

[Enhancement of the antifibrillatory efficacy of quinidine in atrial fibrillation by verapamil (author's transl)].

We reported recently that in patients suffering from atrial fibrillation and being refractory to antifibrillatory therapy with quinidine conversion to sinus rhythm can often be achieved by additional doses of verapamil. To further evaluate the mechanism of this drug interaction, we studied the effects of quinidine, verapamil and combined quinidine-verapamil on the thresholds for electrically induced atrial repetitive extrasystoles (RET) and fibrillation (AFT). Comparative investigations were performed using the new calcium antagonist diltiazem. Our results show that verapamil provides protection against electrically induced atrial reentry arrhythmias only in combination with quinidine, but fails to exert a protective action when given alone. The increased success rate of conversion to sinus rhythm following combined quinidine-verapamil in patients with atrial fibrillation can be explained by an increase in the RET and AFT. The basic mechanism of this effect is supposed to be due to antiadrenergic properties of verapamil. In contrast to verapamil, diltiazen lacks the ability to increase RET and AFT in the presence of quinidine; diltiazen therefore cannot be expected to increase the antifibrillatory efficacy of quinidine in patients with atrial fibrillation.

Animals↗
PubMed1981

Sympathomimetic and cardiodepressant effects of acebutolol, oxprenolol, pindolol, and propranolol. A comparative study on changes in hemodynamics, contractility, heart rate, and AV-conduction time at therapeutic doses.

The present study was undertaken in order to obtain further informations on non-beta-antiadrenergic properties of the four beta-sympatholytic agents acebutolol, oxprenolol, pindolol, and propranolol. Standardized experiments were performed using a chronically reserpinized canine preparation for the assessment of dose-response curves of changes in hemodynamics, left ventricular contractility, heart rate, AV-conduction time, and myocardial oxygen consumption especially at therapeutic doses. Our results show that acebutolol and oxprenolol, at doses clinically recommended, exert moderate positive inotropic effects but do not influence heart rate significantly. Pindolol has a strong both positive chronotropic and inotropic efficacy, even at small therapeutic doses. Propranolol produces neither chronotropic nor inotropic effects. In contrast to the literature acebutolol exerts direct cardiodepression at doses clinically used, whereas oxprenolol, pindolol, at propranolol have no direct cardiodepressant properties at those doses. Thus the relationship between the dose requirements for chronotropic and inotropic sympathomimetic effects differs for each beta-sympatholytic agents, and in may prove impossible to get an order of intrinsic sympathomimetic potency of beta-blockers comparing dose-response curves of heart rate changes only. As shown in the case of acebutolol, direct cardiodepression of beta-sympatholytic agents may occur at therapeutic doses.

Acebutolol↗
PubMed1981

[The effect of nicotine on the hemodynamics and oxygen consumption of the heart following acute and chronic sympathetic blockade and atropine].

In 22 artificially ventilated morphine-urethane-chloralose anesthetized dogs (body weight 17--25 kg) the effects of nicotine (0.01 mg/kg x min i.v. over a 5-min period) on the time course of changes in hemodynamics, contractility and oxygen consumption of the heart were examined before and after acute and chronic pretreatment with sympatholytic agents and with atropine. The purpose of this study was to evaluate quantitatively the different components of the hemodynamic overall effect of nicotine in the intact animal. Our results demonstrate that the increase in myocardial oxygen consumption is mediated predominantly by indirect effects of nicotine (adrenergic and vagal effects). In doses comparable to the nicotine consumption of cigarette smokers, this increase is about 20%. Comparatively, the increase in myocardial oxygen consumption mediated by direct nicotine effects is quantitatively small.

Animals↗
PubMed1981

[Antiarrhythmic therapy with flecainide in acute experimental myocardial infarction (author's transl)].

Clinical and experimental studies indicate that ventricular arrhythmias, especially ventricular fibrillation, are in almost all cases the mechanism for sudden death occurring during the first 24 hours after the onset of an ischaemic myocardial event. Therefore a higher survival rate seems to depend on advances in antiarrhythmic therapy. The present study investigates the efficacy of the new local anaesthetic compound Flecainide in reducing or preventing ventricular arrhythmias and primary ventricular fibrillation, using a standardized experimental canine preparation. Our findings demonstrate that ventricular arrhythmias due to severe transmural myocardial infarction are reduced by 80-90% following the application of Flecainide. In some cases a complete abolition of the arrhythmias can be observed. The striking reduction in ventricular ectopics includes decreases in ventricular salves and R-on-T phenomena, which may lead to sudden death by precipitating ventricular fibrillation. The beneficial antiarrhythmic and antifibrillatory actions of Flecainide affect only the arrhythmias resulting from transmural necrosis of the myocardium ("in-hospital arrhythmias", 2nd-phase arrhythmias"), whereas the incidence of early ventricular arrhythmias, especially ventricular fibrillation occurring in the very inception of myocardial ischaemia ("pre-hospital arrhythmias", "1st-phase arrhythmias") is not prevented. Changes in hemodynamics and contractility due to Flecainide are not severe, even in myocardial infarction. Thus, our results indicate that the application of Flecainide in acute myocardial infarction in man may be successful in reducing therapy-resistant ventricular dysrhythmias.

Animals↗
PubMed1980

[Effects of sulfinpyrazone on early ventricular fibrillation and 2d-phase arrhythmias in acute myocardial infarction (author's transl)].

Clinical and experimental studies indicate that ventricular arrhythmias, mainly ventricular fibrillation, are responsible for sudden cardiac death. A recent double-blind multicenter trial ("Anturane Reinfarction Trial") showed that the incidence of sudden cardiac death was reduced in Sulfinpyrazone-treated patients after acute myocardial infarction compared with the placebo group, although the rate of reinfarctions was not diminished. We investigated the efficacy of Sulfinpyrazone on the reduction and prevention of ventricular arrhythmias and primary ventricular fibrillation, utilizing a standardized experimental canine preparation. At normal therapeutic and at high cumulative doses of the drug, a reduction in ventricular arrhythmias within the first 24 hours after coronary occlusion could not be observed. Sulfinpyrazone failed also to alter the ventricular vulnerability to fibrillation in the very early myocardial infarction period. Furthermore, haemodynamics, contractility and oxygen consumption of the heart were not changed. These experimental findings show that the reduction in sudden cardiac deaths in Sulfinpyrazone-treated patients cannot be attributed to antiarrhythmic effects of the drug. Further research is needed to delineate the mechanism of action of Sulfinpyrazone as reported by the Anturane Reinfarction Trial Research Group.

Animals↗