Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prenalterol is an orally active cardioselective beta agonist, with a long half-life. Previous studies have confirmed its inotropic activity following intravenous infusion in patients with heart failure. It has little chronotropic activity and no significant arrhythmogenicity. We have studied the response to sustained-release oral prenalterol given over four weeks at doses of 20, 40, 100, and 200 mg daily in 10 patients with New York Heart Association class II and III heart failure due to ischemic heart disease. All were in sinus rhythm and already receiving diuretics and digoxin. The drug was well tolerated and without side effects. Nine patients showed a dose-related improvement in their exercise tolerance as measured on the treadmill, up to a dose of 100 mg daily, with a significant increase in estimated oxygen uptake. There was a dose-related reduction in maximum heart rate, systolic blood pressure, and rate-pressure product during exercise, which is suggestive of a reduction in myocardial oxygen consumption. We conclude that prenalterol improves exercise tolerance without any significant cardiovascular or other side effects, and produces a clinically relevant and sustained improvement in patients with chronic heart failure. M-mode echocardiographic measurements of left ventricular dimension and function at rest did not show any change during the study.
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PMID:A dose response study with oral prenalterol in patients with chronic congestive cardiac failure. 670 84

The hemodynamic, hormonal and electrolyte effects of prenalterol, a synthetic selective beta 1 agonist, were studied in six patients with New York Heart Association functional class II and III heart failure. Prenalterol was infused incrementally at 60, 120 and 240 nmol/min, each rate for 24 hours, producing steady-state plasma prenalterol levels of 52 +/- 3, 121 +/- 6 and 194 +/- 9 nmol/1, respectively (mean +/- SEM). Hemodynamic and hormonal measurements were performed before, during and after prenalterol administration under conditions of constant body posture and a regulated intake of dietary sodium and potassium. Prenalterol induced a statistically significant increase in cardiac index (from 2.6 +/- 0.2 to 3.1 +/- 0.3 1/min/m2), with parallel increases in stroke index (from 28 +/- 2 to 34 +/- 2 ml/beat/m2). Forearm blood flow measurements increased (from 2.9 +/- 0.5 to 4.1 +/- 0.6 ml/min/100 g), while calculated systemic vascular resistance fell, as did pulmonary capillary wedge pressure (from 13.7 +/- 1.6 to 10.5 +/- 1.7 mm Hg). The drug did not alter heart rate, arterial pressure, right heart pressures or the frequency of ventricular premature beats. Prenalterol increased plasma renin activity (from 2.9 +/- 0.8 to 6.6 +/- 1.8 nmol/1/hour), angiotensin II (from 59 +/- 12 to 89 +/- 22 pmol/1), urinary aldosterone excretion (from 41 +/- 10 to 78 +/- 34 nmol/day) and plasma insulin (from 10.6 +/- 2.2 to 19.8 +/- 3.9 mU/1). Circulating catecholamines, cortisol, glucose, glucagon or pancreatic polypeptide did not change. Dose-response studies in five patients showed dose-dependent increments in hemodynamic variables, while hormonal changes plateaued at the second dose level. We conclude that prenalterol infusion augments myocardial contractility, reduces systemic vascular resistance, and stimulates insulin release and the renin-angiotensin-aldosterone system.
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PMID:Hemodynamic, hormonal and electrolyte responses to prenalterol infusion in heart failure. 682 3


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