Dose–dependent haemodynamic response to prenalterol in patients with congestive heart failure

Leinberger, H.; Mäurer, W; Haueisen, H.; Schuler, Gerhard; Kübler, W.

doi:10.1111/j.0954-6820.1982.tb00854.x

Cited by 2 publications

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“…This may be due to differences in the sensitivity of p receptors (Thomas & Marks 1978;Ariniego et al 1979;Kupper et al 1983). It has been demonstrated that patients with high plasma catecholamine levels as in severe cardiac failure do not increase heart rate after prenalterol intravenously (Leinberger et al 1982). The increase in heart rate showed marked interindividual variability but was positively correlated to log plasma concentration (Carlsson et al 1977;Rsnn et al 1980).…”

Section: Discussionmentioning

confidence: 99%

The Immediate Haemodynamic and Electrophysiological Response to Prenalterol during Fixed Rate Pacing in Patients with Chronic Ischaemic Heart Disease

Sire¹,

Amlie²,

Simonsen³

1986

Acta Pharmacologica et Toxicologica

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The immediate haemodynamic and electrophysiologic effects of intravenous prenalterol 2.5–75μg/kg in patients with coronary heart disease without clinical heart failure were investigated during fixed rate atrial pacing. Right ventricular peak dP/dt increased pronounced and serum concentration dependent after prenalterol concomitant with an increase in stroke volume and a moderate decrease in peripheral vascular resistance. The effects on haemodynamics after prenalterol were thus serum concentration dependent but with marked interindividual variation. AV nodal conduction velocity increased significantly. It is concluded that prenalterol possess pronounced inotropic properties. The haemodynamic response to prenalterol intravenously is to a lesser degree dependent on the chronotropic effects of the drug and it is often unpredictable.

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Section: Discussionmentioning

confidence: 99%

The Immediate Haemodynamic and Electrophysiological Response to Prenalterol during Fixed Rate Pacing in Patients with Chronic Ischaemic Heart Disease

Sire¹,

Amlie²,

Simonsen³

1986

Acta Pharmacologica et Toxicologica

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Prenalterol

Vickers

1984

Cardiovascular Drug Reviews

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Prenalterol (H133/22) is the hydrochloride salt of the levorotatory (-) isomer of l-(4-hydroxyphenoxy)-3-isopropyl-amino-2-propanol (Fig. 1). The compound has a molecular weight of 261.75 and a melting point of 125" C. It is freely soluble in water. The pKa values are 9.5 (amine) and 10.0 (phenolic).Prenalterol has been characterized as a selective PI-adrenoceptor agonist. Pharmacologic studies have shown that it has positive inotropic as well as chronotropic effects. At lower doses, the positive inotropic effect is associated with a minimal effect on heart rate; at effective inotropic doses, the drug appears to have less tendency to cause arrhythmias than either cardiac glycosides or other sympathomimetic amines. Clinical studies have shown the utility of prenalterol as a padrenoceptor agonist. It is anticipated that prenalterol will be used in the management of patients with congestive heart failure, myocardial ischemia, and coronary artery disease and in postoperative cardiac surgery. ANIMAL PHARMACOLOGY Cardiovascular Effects lnotropic and Chronotropic PropertiesThe pharmacologic activity of several p-adrenoceptor agonists, including prenalterol, was studied in the norepinephrine-depleted anesthetized cat. Prenalterol increased heart rate but did not dilate the hindlimb vasculature. Isoproterenol and terbutaline caused a dose-dependent increase in heart rate as well as a dilation of the hindlimb vasculature. The ratios of the ED5,, for vasodilation to the ED50 for heart rate for isoproterenol, terbutaline, and prenalterol were 0.3, 0.1, and >600, respectively. These values indicate that prenalterol has a high degree of selectivity for cardiac P-adrenoceptors, while isoproterenol and particularly terbutaline have a higher affinity for vascular p-adrenoceptors (13). PRENALTEROLPrenalterol and terbutaline differed in their relative inotropic and chronotropic activities in the cat. The ratios of the ED5& for heart rate to the maximum dpldt for prenalterol and terbutaline were 0.93 and 0.16, respectively. The ED,, ratio for isoproterenol did not differ significantly from that for prenalterol. Thus it was possible to differentiate between P-agonists with primarily a positive chronotropic or inotropic effect. Terbutaline, a @,-selective agonist, at 36 nmoles/kg i.v., increased heart rate to a greater extent than the contractile force; prenalterol, a PIselective agonist, at 9 nmolesikg i.v., had equal positive inotropic and chronotropic effects.It was hypothesized that both PIand P,-adrenoceptors are present in the sinoatrial (SA) node and in the myocardium of the ventricles, but that their relative distribution differed. The ratio of the 6,to the P,-adrenoceptors appeared to be higher in the ventricle than in the SA node. Terbutaline, therefore, a @,-selective agonist, was more effective on the SA node than on the ventricle, and the chronotropic response to terbutaline was more pronounced than the inotropic response. Prenalterol, on the other hand, produces equal chronotropic and inotropic effects because of its hi...

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Dose–dependent haemodynamic response to prenalterol in patients with congestive heart failure

Cited by 2 publications

References 0 publications

The Immediate Haemodynamic and Electrophysiological Response to Prenalterol during Fixed Rate Pacing in Patients with Chronic Ischaemic Heart Disease

The Immediate Haemodynamic and Electrophysiological Response to Prenalterol during Fixed Rate Pacing in Patients with Chronic Ischaemic Heart Disease

Prenalterol

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