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At least 1,405 records · Page 78Linked to original sources
PubMed1981

Hemodynamic actions of prenalterol in severe congestive heart failure due to chronic coronary disease.

To provide improved inotropic agents for enhanced therapy of severe congestive heart failure (CHF), the hemodynamic efficacy of prenalterol (PN), a recently developed cardioselective beta-1 receptor agonist, was evaluated by cardiac catheterization in nine patients with refractory CHF due to chronic coronary disease. PN (4.8 mg intravenously) markedly augmented the cardiac index from 1.9 to 2.6 L/min/m2 (p less than 0.01) and substantially elevated stroke index from 24 to 30 ml/beat/m2 (p less than 0.001). Additionally, PN raised stroke work index 21 to 26 gm.m/m2 (p less than 0.005) and decreased total systemic vascular resistance from 1,702 to 1,260 dynes-sec cm(-5) (p less than 0.001). Concomitantly, heart rate, mean blood pressure, and left ventricular filling pressure were unaltered ( p greater than 0.05). Importantly, the heart rate-systolic blood pressure product was unchanged (p less than 0.05), and precipitation of cardiac dysrhythmias or myocardial ischemia was not observed. Thus PN produced considerable improvement of depressed cardiocirculatory performance without untoward effects and thereby appears a valuable new cardiotonic in the clinical management of severe low output ventricular dysfunction.

Aged↗
PubMed1981

Clinical results with prenalterol in patients with heart failure.

The hemodynamic effect of 75 to 225 microgram/kg prenalterol (PNL) intravenously were studied at rest and during exercise in eight patients with chronic congestive heart failure (CHF) after myocardial infraction (three patients), valvular surgery (three patients), and congestive cardiomyopathy (two patients). All head New York Health Association functional class III and IV CHF and were receiving digitalis and diuretics. With PNL at rest, left ventricular filling pressure (LVFP) fell from 17 to 12 mm Hg, cardiac index (CI) rose from 2.1 to 2.9 L/min/m2, heart rate (HR) increased mildly, systemic vascular resistance (SVR) declined moderately, and peripheral arterial pressure was unchanged. During PNL exercise compared with control, LVFP rise was less and CI, HR, and SVR responses were similar; dyspnea and angina were reduced in most patients. The eight patients were than given PNL orally, 30 to 200 mg/day, versus placebo for 6 days with comparative evaluation by echocardiogram, systolic time intervals (STI), exercise test, and continuous ECG. With PNL orally five of eight patients improved symptomatically, ejection fraction increased from 0.44 to 0.53, and STI preejection period shortened by 10 msec, without change in resting HR or systemic arterial blood pressure. The incidence of ventricular premature beats was not increased. PNL orally vs placebo exercise capacity increased 10%. Thus PNL may be of value for long-term CHF treatment in addition to conventional therapy.

Administration, Oral↗
PubMed1984

Prenalterol in cardiogenic shock following acute myocardial infarction.

Eleven patients with cardiogenic shock following acute myocardial infarction (AMI) have been treated with prenalterol. This drug was administered in seven patients once dobutamine or dopamine proved to be ineffective or poorly effective, and it was the first inotropic drug employed in four patients. Therapeutic dose of intravenous infusion ranged from 2.2 to 18 micrograms/kg/min (mean dose: 7 micrograms/kg/min), and was maintained for 2 to 4 hours. Since two patients received the infusion on two different occasions, a total of 13 cases were considered for statistical analysis. Prenalterol produced an increase in cardiac index (p less than 0.01), mean aortic pressure (p less than 0.02), net work index (p less than 0.01), net/stroke work index (p less than 0.01), pressure rate product (p less than 0.05), and myocardial perfusion gradient (p less than 0.02). It decreased systemic (p less than 0.02) and pulmonary (p less than 0.01) vascular resistances, pulmonary artery (p less than 0.01) and pulmonary capillary (p less than 0.05) pressures. Heart rate and right atrial pressure were not significantly changed. The drug acted as a relatively selective inotropic agent without a chronotropic effect and with minimal peripheral actions. It was effective in seven patients and ineffective in four patients. Thus prenalterol appears to be a useful drug in cardiogenic shock and further studies are warranted.

Adrenergic beta-Agonists↗
PubMed1984

Hemodynamic trial of sequential treatment with diuretic, vasodilator, and positive inotropic drugs in left ventricular failure following acute myocardial infarction.

The circulatory effects induced by two sequential intravenous treatment programs with a diuretic, arteriolar or venodilator , and a positive inotropic drug were studied in a randomized between-group trial in 20 male patients with radiographic and hemodynamic evidence of left ventricular (LV) failure following acute myocardial infarction (AMI). Furosemide induced a substantial diuresis in both groups of patients, in association with reductions in LV filling pressure (p less than 0.01) and cardiac output (p less than 0.05), without significant change in heart rate or systemic arterial pressure. The addition of isosorbide dinitrate was followed by reductions in the systemic arterial (p less than 0.01) and LV filling pressures (p less than 0.01) without significant change in the heart rate or cardiac output. Hydralazine after furosemide reduced systemic vascular resistance (p less than 0.01), but the fall in mean blood pressure (p less than 0.01) was limited by the increase in cardiac output (p less than 0.01); heart rate was also increased (p less than 0.01) and LV filling pressure fell (p less than 0.05). The final addition of the beta-1 adrenoceptor agonist, prenalterol, increased systemic arterial systolic pressure (p less than 0.05), cardiac output (p less than 0.05), and heart rate (p less than 0.01), and reduced systemic vascular resistance (p less than 0.01) in both groups; these changes were greatest in those pretreated with furosemide and isosorbide dinitrate. In both treatment pathways compared with control the reductions in systemic vascular resistance and left heart filling pressure were accompanied by increases in heart rate and cardiac output without substantial changes in systemic blood pressure. Which of these hemodynamic pathways offers the optimum prognosis awaits further study.

Adrenergic beta-Agonists↗
PubMed1981

Hemodynamic effects of intravenous prenalterol in severe heart failure.

Nine patients with chronic severe low output heart failure (radionuclide left ventricular ejection fraction 17 +/- 5 percent [mean +/- standard deviation], left ventricular filling pressure 26 +/- 6 mm Hg, cardiac index 1.9 +/- 0.4 liters/min per m2, left ventricular stroke work index 18 +/- 6 g-m/m2) from various causes were treated with intravenous prenalterol (a new catecholamine-like inotropic agent) in doses of 1,4 and 8 mg. Significant hemodynamic improvement occurred as measured by increased left ventricular ejection fraction (to 26 +/- 4 percent), decreased left ventricular filling pressure (to 21 +/- 8 mm Hg) and increased cardiac index (to 2.4 +/- 0.6 liters/min per m2) and left ventricular stroke work index (to 25 +/- 8 g-m/m2). Significant increases in heart rate (from 87 +/- 18 to 91 +/- 18 beats/min) and mean systemic arterial pressure (from 87 +/- 8 to 92 +/- 7 mm Hg) also occurred. Peak hemodynamic response occurred at various doses. Significant adverse effects associated with prenalterol consisted of increased ventricular ectopic beats in two patients and asymptomatic ventricular tachycardia in two patients. Thus, intravenous prenalterol produces hemodynamic improvement in patients with a chronic severe low output state but may be associated with increased ventricular ectopic activity.

Aged↗
PubMed1985

Prevention of epinephrine-induced hypokalemia by nonselective beta blockers.

Experimental evidence is presented that activation of beta 2 adrenoreceptors causes a dose-dependent decrease in plasma potassium, probably by shifting potassium into the cell. By this mechanism epinephrine may cause hypokalemia and predispose to cardiac arrhythmias. Prevention of these effects by nonselective beta blockers may contribute to the cardioprotective action of these drugs.

Adrenergic beta-Antagonists↗
PubMed1984

Intravenous and oral prenalterol in congestive heart failure. Effects on systemic and coronary hemodynamics and myocardial catecholamine balance.

Systemic and coronary hemodynamic effects of prenalterol, a beta-1 receptor agonist, were determined in patients with chronic congestive heart failure, initially after intravenous administration (10 patients) and then after oral administration (eight patients). Cardiac index increased by 33 percent and 30 percent after intravenous and oral prenalterol, respectively. The increase in stroke volume index and stroke work index and decrease in pulmonary capillary wedge pressure and systemic vascular resistance were not significant. Myocardial oxygen consumption and coronary sinus blood flow increased in the majority of patients, although these changes were not statistically significant. There were no significant changes in transmyocardial norepinephrine or epinephrine balance. The systemic and coronary hemodynamic effects of both intravenous and oral prenalterol were similar. Major side effects included sudden death (two patients) and hypotension and bradycardia (three patients) during oral prenalterol treatment. It is concluded that improved left ventricular function following both intravenous and oral prenalterol may be associated with increased myocardial oxygen consumption, and serious adverse effects may occur during prenalterol therapy.

Administration, Oral↗
PubMed1977

Mechanical and metabolic effects of insulin on newborn lamb myocardium.

The effects of insulin on myocardial contractility (MC) and metabolism were studied in 18 newborn lambs. Cardiac work and rate were kept constant. Following insulin (80 units, intravenously), contractility increased and remained elevated for 1 hour. This was not prevented by beta blockade or glucose infusion. Myocardial extraction and uptake of glucose and nonesterified fatty acid (NEFA) increased, the arterial concentration of both decreased. But after glucose fell to less than 20 per cent of control, uptake of both glucose and NEFA declined as did MC. It is concluded that in the neonate insulin increases MC as well as substrate uptake.

Animals↗
PubMed1984

Inhomogeneities in glycoprotein cytochemistry of secretory granules in rat-parotid acinar cells after selective beta 1-adrenoceptor stimulation.

The distribution of periodate-positive glycoproteins was studied in parotid acinar cells of the rat after stimulation with the specific beta 1-adrenoceptor agonist prenalterol. After two weeks of daily injections, the majority of secretory granules were larger, less electron dense, and often exhibited a bipartite or pleomorphic PA-CrA-silver staining pattern. A great variation in the staining pattern of the secretory granules was seen among different cells but, within any individual cell, most granules displayed a similar pattern. The staining reaction suggests a mucoid transformation of the granules, or a reorganization of the glycoproteins within the granules. The variation among cells in the staining pattern of granules may suggest that there are different populations of acinar cells or of secretory granules.

Adrenergic beta-Agonists↗