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PubMed1989

Drug-induced immune-complex disease.

A range of drugs including hydralazine, isoniazid, procainamide and penicillamine cause toxic side effects which resemble systemic lupus erythematosus (SLE). Deficiencies of C1, C4 and C2 are associated with idiopathic SLE, and these defects may compromise the ability of the patient to deal with immune complexes. Immune complexes with protein as antigen, such as has been reported to be diagnostic of procainamide-induced SLE, interact more with the C4A isotype of C4 than the C4B isotype. It is shown that hydralazine, isoniazid and penicillamine inhibit the covalent binding of C4 to a complement-activating surface and that the drugs themselves become covalently bound to C4. For each of these drugs, C4A is inhibited more than C4B, and it is suggested that this is an important contributory factor in the development of the toxic side effects to these drugs involving immune-complex deposition. For procainamide, it is shown that the hydroxylamine metabolite rather than the drug itself inhibits the covalent binding reaction of C4. Hydralazine, isoniazid and procainamide are metabolised by the polymorphic N-acetyltransferase, and slow acetylators are at increased risk of drug-induced lupus. For procainamide, oxidation to the hydroxylamine form is an alternative metabolic route of increased importance in slow acetylators, and it is suggested that investigation of C4 type in susceptible patients could provide a means of identifying those at greatest risk of immunotoxicity.

Humans↗
PubMed1976

Toward preventing coronary death from ventricular fibrillation.

Sudden coronary death from ventricular fibrillation is the biggest and possibly the most remediable of the major public health problems at the moment. Most of those liable to sudden death can be identified and it is possible that by the use of beta-adrenergic blocking or other antiarrhythmic drugs, by reducing the consumption of cigarettes and perhaps, by different therapies for hypertension, a substantial proportion of coronary deaths might be prevented or, at least, postponed.

Adult↗
PubMed1981

Hemodynamic effects of atrial pacing and prenalterol infusion in patients taking beta-adrenergic blocking drugs.

Prenalterol, a beta-adrenergic agonist, was given to nine patients with angiographically proved coronary artery disease. Subjects were studied during chronic beta-adrenergic blockade. The adequacy of blockade was assessed by the exercise heart rate response and by plasma concentrations of blocking agents. After incremental doses of 2.5 mg, 5.0 mg and 7.5 mg of prenalterol, heart rate was increased by 20%, 24% and 38%, respectively, and left ventricular dP/dt max by 55%, 73% and 61%, respectively. Systolic and diastolic blood pressures did not change significantly; pulmonary artery wedge pressure fell from 10 +/- 0.5 mm Hg to 7.1 +/- 0.9 and 6.7 +/- 0.7 mm Hg after 2.5 mg and 5.0 mg, respectively (p less than 0.01 for both). The net inotropic response to prenalterol was assessed, independent of the chronotropic response, using incremental atrial pacing before and after drug infusion. At identical heart rates, left ventricular dP/dt max increased by 40%, 49% and 48% after 2.5 mg, 5.0 mg and 7.5 mg, respectively. Left ventricular cineangiography before and after infusion showed an increase in ejection fraction from 0.73 +/- 0.02 to 0.83 +/- 0.03 (p less than 0.001). Plasma prenalterol concentration estimations demonstrated a clear, dose-related inotropic response, the level of response in each patient being largely determined by the degree of beta-adrenergic blockade at the time of the study.

Adrenergic beta-Antagonists↗
PubMed1983

Hemodynamic, hormonal and electrolyte responses to prenalterol infusion in heart failure.

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.

Dose-Response Relationship, Drug↗
PubMed1984

Long-term hemodynamic effects of prenalterol in patients with severe congestive heart failure.

In a controlled, randomized, double-blind study we investigated the long-term effects of the beta 1-adrenoceptor agonist prenalterol in 16 patients with severe congestive heart failure (NYHA class III or IV). Previous to and 1 week, 3 months, and 6 months after continuous oral intake of 40 to 120 mg prenalterol a day, catheterization of the right heart combined with an ergometer test was carried out; M mode and two dimensional echocardiograms as well as systolic time intervals were also recorded. With prenalterol the heart rate increased within 1 week from 81 +/- 7 to 90 +/- 7 beats/min (mean +/- SD) (p less than .05) and remained increased after 3 months (93 +/- 9 beats/min, p less than .01) and 6 months (91 +/- 6 beats/min, p less than .05). After 1 week the cardiac index rose from 2.7 +/- 0.7 to 3.3 +/- 0.7 l/min/m2 (p less than .01), and after 3 and 6 months it fell again to 3.0 +/- 0.9 l/min/m2 and 2.9 +/- 0.7 l/min/m2, respectively. In the ergometer test the improvement in performance was not significant. The mean velocity of circumferential fiber shortening initially increased from 0.58 +/- 0.20 to 0.79 +/- 0.28 circumferences/sec (p less than .01), but dropped after 3 months to 0.62 +/- 0.31 circumferences/sec. The ejection fraction determined from the two-dimensional echocardiogram rose after 1 week from 20 +/- 10 to 27 +/- 12% (p less than .05), but decreased again after 3 months (23 +/- 11%) and 6 months (20 +/- 10%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1984

Beta-adrenergic stimulation of the failing ventricle: a double-blind, randomized trial of sustained oral therapy with prenalterol.

Eleven patients with severe left ventricular impairment (mean ejection fraction 24%) and moderate impairment of exercise tolerance underwent a double-blind, placebo-controlled, cross-over trial of the orally administered beta-agonist prenalterol. Exercise hemodynamics and tolerance were measured during bicycle and treadmill exercise after 2 weeks of therapy with placebo or prenalterol. Cardiac index, ejection fraction, and stroke work index were not improved and exercise duration and peak oxygen consumption were not significantly different during the two treatments. During prenalterol treatment heart rate during exercise was consistently reduced. These results show that prolonged therapy with prenalterol does not improve hemodynamics or exercise tolerance and is associated with a diminished heart rate response to exercise.

Administration, Oral↗
PubMed1976

Hierarchy of ventricular pacemakers.

To characterize the pattern of pacemaker dominance in the ventricular specialized conduction system (VSCS), escape ventricular pacemakers were localized and quantified in vivo and in virto, in normal hearts and in hearts 24 hours after myocardial infarction. Excape pacemaker foci were localized in vivo during vagally induced atrial arrest by means of electrograms recorded from the His bundle and proximal bundle branches and standard electrocardiographic limb leads. The VSCS was isolated using a modified Elizari preparation or preparations of each bundle branch. Peacemakers were located by extra- and intracellular recordings. Escape pacemaker foci in vivo were always in the proximal conduction system, usually the left bundle branch. The rate was 43+/-11 (mean+/-SD) beats/min. After beta-adrenergic blockade, the mean rate fell to 31+/-10 beats/min, but there were no shifts in pacemaker location. In the infarcted hearts, pacemakers were located in the peripheral left bundle branch. The mean rate was 146+/-20 beats/min. In isolated normal preparations, the dominant pacemakers usually were in the His bundle, firing at a mean rate of 43+/-10 beats/min. The rates of pacemakers diminished with distal progression. In infarcted hearts, the pacemakers invariably were in the infarct zone. The mean firing rates were not influenced by beta-adrenergic blockade. The results indicate that the dominant pacemakers are normally in the very proximal VSCS, but after myocardial infarction pacemaker dominance is shifted into the infarct. Distribution of pacemaker dominance is independent of sympathetic influence.

Animals↗