Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Practolol”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,585 records · Page 88Linked to original sources
PubMed1982

The hemodynamic actions of prenalterol in left ventricular failure.

The hemodynamic effects of prenalterol, a parenteral cardioselective beta 1-receptor agonist, were evaluated by cardiac catheterization in patients with refractory severe congestive heart failure (CHF). Prenalterol (PN) (4 mg i.v.) did not alter (p greater than 0.05) heart rate (HR), mean blood pressure (MBP) or left ventricular filling pressure (LVFP). Concomitantly PN markedly augmented cardiac index (CI) from 1.9 to 2.6 l/min/m2 (p less than 0.01) and substantially elevated stroke index (SI) from 24 to 30 ml/beta/m2 (p less than 0.001). In addition PN raised stroke work index (SWI) from 21 to 26 g . m/m2 (p less than 0.005) and decreased total systemic vascular resistance (TSVR) from 1702 to 1260 dyn . s. cm-5 (p less than 0.001). An important finding was that the heart rate x systolic blood pressure product was unchanged (p greater than 0.05) and precipitation of cardiac dysrhythmias or myocardial ischemia were not observed. Further PN 1 mg, 4 mg and 8 mg i.v. was sequentially injected and peak hemodynamic effects were determined 10 min after drug administration. PN 1 mg raised CI from 2.1 to 2.5 1/min/m2 (p less than 0.01), elevated SI from 24 to 29 ml/beat/m2 (p less than 0.01), and augmented SWI from 21 to 25 g . m/m2 (p less than 0.01), however, TSVR declined from 1702 to 1392 dyn . s. cm-5. Subsequent incremental PN doses of 4 and 8 mg did not provide (p greater than 0.05) additional enhancement of cardiac function. Thus, prenalterol produced markedly beneficial enhancement of cardiocirculatory function without untoward effects and may be useful in the management of patients with severe congestive heart failure. Moreover, dose-response analysis indicates these salutary improvements can be maximally produced by the small dose of 1 mg obviating the need for larger doses.

Adrenergic beta-Agonists↗
PubMed1982

Effect of intravenous prenalterol on haemodynamics and myocardial lactate extraction in patients with left ventricular failure.

To assess the immediate haemodynamic and myocardial metabolic effects of the beta 1-agonist prenalterol, we studied by cardiac catheterisation the response to 50 and 100 micrograms/kg given intravenously in 16 patients with congestive heart failure secondary to coronary artery disease or non-ischaemic cardiomyopathy. At peak effect, cardiac index increased from 2.6 +/- 0.5 to 3.2 +/- 0.8 1/min/m2 (mean +/- SD) p less than 0.001); peak rate of left ventricular pressure development rose from 963 +/- 242 to 1355 +/- 411 mm Hg per second (p less than 0.001); left ventricular end-diastolic pressure fell from 27 +/- 6 to 13 +/- 7 mm Hg (p less than 0.001); coronary sinus blood flow increased from 120 +/- 39 to 147 +/- 55 ml/min (p less than 0.01); myocardial oxygen consumption was augmented from 12.9 +/- 3.9 to 15.7 +/- 5.8 ml/min (p less than 0.001); and heart rate increased slightly (76 +/- 12 to 86 +/- 14 beats per minute, p less than 0.05). No significant changes occurred in left ventricular systolic pressure, stroke volume index, myocardial lactate extraction rate, myocardial arteriovenous oxygen difference and no patient developed angina, ECG-changes or ventricular arrhythmias. Infusion of prenalterol effectively improved the haemodynamic function and cardiac metabolism in congestive cardiomyopathy.

Adrenergic beta-Agonists↗
PubMed1982

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

The effect of three doses of prenalterol, 12.5, 25 and 50 micrograms, on cardiac index (CI), pulmonary artery pressure (PAP), heart rate (HR), and stroke volume index (SVI) was investigated in 18 patients with congestive heart failure (CHF). Twelve patients received only prenalterol, while 6 patients received prenalterol 1 hour after an oral dose of hydralazine and isosorbid dinitrate. In 7 out of 12 patients a dose-dependent increase in HR was observed. The response of HR was inversely correlated to resting catecholamine levels; patients with high resting catecholamines--these are patients with severe CHF--did not show any increase in HR. CI increased in 8 out of 12 patients (average 1 . 1/min m) and SVI in 5 out of 12 patients. This inconsistent response was not dependent on left ventricular ejection fraction or plasma catecholamines at rest. Pretreatment with vasodilators did not improve the haemodynamic response to prenalterol. Four out of 17 patients demonstrated an increase in severity of arrhythmias suggestive of arrhythmogenic properties of prenalterol.

Administration, Oral↗
PubMed1982

Effects of i.v. prenalterol in patients with severe cardiac failure at rest and during exercise.

Prenalterol administration (150 micrograms/kg i.v.) exerted beneficial effects on resting and/or exercise cardiac performance in patients with congestive cardiomyopathy (n = 12) and 1 patient with hypertensive heart disease (= group I, n = 13), while the haemodynamic response in patients with severe coronary heart disease (n=3) or cor pulmonale (n = 1) was non-uniform. At rest mean right and left ventricular filling pressures decreased by 26 and 19% (p less than 0.02 and p less than 0.02), respectively, while stroke volume increased by 8% (p less than 0.05), cardiac index by 25% (p less than 0.01) and heart rate by 15% (p less than 0.005) 5 min after prenalterol administration in group I. During exercise there was no further increase in heart rate, while filling pressures decreased and cardiac index increased significantly compared to control exercise. This typical inotropic response to prenalterol was observed in fully digitalised patients. Maximal effects occurred about 15 min after i.v. administration.

Adrenergic beta-Agonists↗
PubMed1983

Massive metoprolol poisoning treated with prenalterol.

A case of massive metoprolol poisoning (50 g) is described. Clinical signs included coma, seizures, hypoventilation, unmeasurable blood pressure, nodal bradycardia, and metabolic acidosis. Treatment comprised intubation, assisted ventilation, gastric lavage, atropine, bicarbonate, glucagon and repeated doses of prenalterol (a total of 160 mg over 15 hours). Prenalterol dosage was simple and could be guided by blood pressure response. Pacemaker treatment was not required. Ethanol concentration was 50 mmol/l (2.4%) on admission. Plasma metoprolol was 68 mumol/l (18 000 ng/ml) 2 hours after admission. The patient was awake after 15 hours.

Adult↗
PubMed1984

Prenalterol as long-term therapy for chronic congestive heart failure. A randomized cross-over trial.

Ten patients with severe chronic congestive heart failure (CHF) due to ischaemic heart disease treated with digitalis and diuretics were randomly allocated to oral treatment with prenalterol (100-200 mg daily in addition to their basal treatment) or to intensified treatment with diuretics in a cross-over trial. A wash-out period of 1-4 weeks was allowed between the two modes of treatment. Most of the patients demonstrated subjective improvement during prenalterol therapy, but this improvement could not be verified objectively by exercise test, echocardiography, chest X-ray or weight measurements. No serious side-effects of either mode of treatment were observed. Heart rate was significantly lower during exercise when the patients were treated with prenalterol than during the control periods or during intensified conventional treatment, indicating that prenalterol acts as a beta-adrenergic receptor blocker during exercise in this patient group. The results indicate that prenalterol is a partial beta-receptor agonist without superior beneficial effects compared to those of intensified conventional treatment in patients with chronic, severe CHF.

Adrenergic beta-Agonists↗
PubMed1985

The possible role of the ancillary properties of beta adrenoceptor antagonists in the management of angina pectoris.

Beta adrenoceptor antagonists are effective in the symptomatic management of angina pectoris. This paper examines critically the possible influence of the ancillary properties of beta 1 selectivity, partial agonism and membrane-stabilizing action on the response in anginal patients. The response is categorized according to experimental, pharmacological and clinical endpoints, placing emphasis on the possible errors which may arise from extrapolation from the former to the latter. It is concluded: That selective beta adrenoceptor antagonism confers limited, but tangible advantages over non-selective antagonists in regard to patients with reversible airways obstruction, and also in the metabolic and haemodynamic response to acute hypoglycaemia. Cardioselectivity does not influence the central haemodynamic response to exercise, but lessens adrenaline-mediated hypertensive responses to smoking and hypoglycaemia. Non-selective partial agonists cause less reduction in resting ventricular function, but their effects on cardiac output during exercise are indistinguishable from full antagonists. Membrane stabilizing properties have a marked influence on the tolerability of these agents in terms of unwanted, nonspecific central nervous system symptoms. Unresolved questions relate to the influence of partial agonism on fatigue, metabolic responses, especially blood lipids and glucose, and the possibility of lesser efficacy in angina compared to full antagonists.

Adrenergic alpha-Antagonists↗
PubMed1985

High-dose prenalterol in beta-blockade intoxication.

This study presents a case of beta-blocker intoxication due to massive overdose of metoprolol (7.5 g). Prenalterol in a dose of 420 mg was given as antidote, in combination with epinephrine in intermittent doses. Resuscitation was performed during 4 hours because of mechanical asystole. The patient regained health in 24 hours after further repeated doses of 30 mg prenalterol. Prenalterol is valuable in the management of toxic doses of beta-blocking drugs, and a titration to extremely high doses of prenalterol might be necessary.

Adult↗
PubMed1981

The effects of intravenous prenalterol on ventricular performance, as assessed by radionuclide ventriculography, in patients with ischaemic heart disease.

1 We have observed the effects of intravenous prenalterol (1 mg and 2 mg) on ventricular performance, assessed by radionuclide ventriculography, in nine patients with ischaemic heart disease with varying degrees of impairment of ventricular performance. In seven of these patients the effects of prenalterol were compared with those of isoprenaline infused at 1 microgram/min. 2 Prenalterol caused no significant increase in heart rate, but systolic blood pressure increased by 26% (P less than 0.002). In contrast, isoprenaline caused heart rate to increase by 22% (P less than 0.02) and diastolic blood pressure to fall by 9% (P less than 0.01). 3 Left ventricular ejection fraction (LVEF) increased with both drugs, but the increase was greater with isoprenaline, as was the fall in the ratio mean ejection time: left ventricular ejection time, which is an index of improved ventricular performance. 4 Because of the increased heart rate and stroke volume produced by isoprenaline, cardiac output increased 45% above control values (P less than 0.001), but the increase in cardiac output after prenalterol did not reach statistical significance. 5 In three patients with very poor ventricular function (LVEF less than 0.30) prenalterol had little effect on ejection fraction, and caused increased regional ventricular dyskinesia. 6 The increase in systolic blood pressure, and therefore cardiac afterload brought about by prenalterol may limit ventricular response. The response might be enhanced by the addition of vasodilator therapy.

Blood Pressure↗
PubMed1987

Conclusiveness of rechallenge in the interpretation of adverse drug reactions.

We here consider the extent to which the presumed correlation between an adverse event and the administration of a particular drug can be reinforced by rechallenge. At first question of terminology is: what is a rechallenge? Rechallenge is often accepted too readily as proof of a causal relationship and clinical examples give illustrations of common misinterpretations. Definitions are proposed to characterize: the outcome of rechallenge; the conditions under which rechallenge is performed. In discussing causality, a sharp distinction is drawn between the outcome per se and the establishment of a causal relationship. Finally, the simple concepts proposed here should permit to establish a typology of rechallenge and to assess, by further experimental or retrospective research, the conclusiveness of rechallenge in interpreting adverse drug reactions.

Child↗