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Biomedical subjects

K Stephan

Publications and source records attributed to K Stephan.

At least 55 records · Page 3Linked to original sources
PubMed1976

[Acute myocardial infarct and pindolol. Effect of a beta sympatholytic with intrinsic sympathomimetic activity on hemodynamics and contractility].

After acute circumscribed myocardial infarction the effects of the beta-sympatholytic agent 1-(indol-4-yl-oxy)-3-isopropyl-amino-propan-2-ol (pindolol; Visken) on hemodynamics and contractility were examined. Hemodynamic changes after application of pindolol are of small extent only. Heart rate shows a rising tendency whereas systolic and diastolic aortic pressure decreases only after higher doses. Left ventricular end-diastolic pressure (LVEDP) does not change remarkably. Cardiac output is reduced by small doses of pindolol and reaches starting values again before the administration of higher doses. Changes of the contractility parameters (dp/dt)max, t-(dp/dtmax, and PEP in the sense of a beta-sympatholysis appear only in the lower range of the doses given. Thus maximum decrease of contractility is 20% measured at (dp/dt)max, which consequently reaches the starting value again. The other contractility parameters change accordingly. These typical dose-response relations between pindolol and contractility parameters are considered to be due to lacking cardiac depressive properties combined with significant so-called positive intrinsic activity. Our results show that no contraindication can be derived from the small influence of pindolol on contractility in acute myocardial infarction.

Animals↗
PubMed1976

[Contractility, pressure and volume reserve of pressure-hypertrophied hearts in situ].

In 18 adult mongrel dogs (24.6 kg) a statistically significant left ventricular hypertrophy (LVH) was induced by chronic aortic coarctation (180 days). In 12 anesthetized dogs (LVH 1) the effect of increasing doses of catecholamines on maximum contractility, expressed by (dp/dt)max, Vpm, t-(dp/dt)max was determined in comparison to a control group (KO 1; N = 6). There was no depression of the acute maximum contractility of hypertrophied hearts compared with the controls, also in respect to other haemodynamic parameters (SV/10 kg, HR, LVEP). In 6 other LVH-dogs (LVH 2) the maximum reached left ventricular pressure - obtained by complete clamping of the ascending aorta - was significantly higher. Either pressure per 100 g left ventricle did not differ significantly.

Animals↗
PubMed1975

Oxygen demand and collateral vessels of the heart. Factors influencing the severity of myocardial ischaemic injury after experimental coronary artery occlusion.

Epicardial electrocardiographic maps were used to assess the effect of heart rate, myocardial contractility, and oxygen need on the severity of myocardial ischaemic injury after acute coronary artery occlusion in dogs. The experimental data indicate statistically significant dependence of the severity of ischaemia on heart rate, contractility, and oxygen need of the heart. These dependences are highly influenced by the spontaneous collateral vessels of the heart.

Animals↗
PubMed1975

[The effect of atenolol on contractility and hemodynamics of the infarcted heart in comparison to propranolol and practolol (author's transl)].

In animals without myocardial infarction the new beta-sympathicolytic agent atenolol (4-[2'-hydroxy-3'-iso-propylaminopropoxy]-phenyl acetamide, ICI 66 082) dose-dependently decreased heart rate, systolic aortic pressure and cardiac output. Coronary mean flow, coronary resistance, stroke volume, left ventricular enddiastolic pressure and total peripheral vascular resistance did not change significantly. Atenolol significantly reduced myocardial contractility, expressed by (dp/dtmax), Vpm, t-(dp/dtmax) and pre-ejection period. Furthermore, the comparative studies in animals with myocardial infarction and concomitant reduced cardial efficiency revealed, that atenolol has neither a positive intrinsic activity as has practolol nor a negative intrinsic activity as has propranolol. The dose-contractility relation of atenolol resembles that of practolol: in low dosages a strong decrease is achieved, in higher dosages no further reduction of the contractility parameters is observed. Because of the strong negative inotropic and blood pressure lowering effect it is suggested to use atenolol only with great caution in patients with reduced cardiac efficiency.

Animals↗