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)

Prazosin, in daily doses of 6--16 mg, was used along with furosemide and polythiazide in 11 hypertensive heart failure patients. Average supine and standing blood pressures were reduced from 180/108 and 171/106 to 130/84 and 135/86, respectively. Average heart rate decreased from 83 to 73 supine and from 84 to 75 standing. Changes in the indices of cardiac function--indlucing the ejection fraction, ejection time, and apical indices--each indicated improvement of left ventricular function. Thus prazosin along with diuretic agents may be particularly useful in the treatment simultaneously of heart failure and of elevated blood pressure with few side effects.
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PMID:Prazosin in hypertension with heart failure. 9 40

In patients with chronic heart failure exercise allows the simultaneous observation of the cardiovascular pathophysiology and the symptoms of these patients. We administered short-term, oral prazosin to 10 patients with severe chronic heart failure. Prazosin increased cardiac output and stroke volume significantly during exercise (both P less than 0.05) but not at rest (both P greater than 0.10). Prazosin decreased the arteriovenous oxygen difference and left ventricular filling pressure significantly during exercise (both P less than 0.05) but not at rest (both P greater than 0.10). There was no significant correlation between prazosin-induced changes at rest and during exercise in cardiac output (r = 0.12), stroke volume (r = 0.02), arteriovenous oxygen difference (r = 0.33) or left ventricular filling pressure (r = 0.43). Prazosin predominantly affects hemodynamics during exercise because its pharmacologic activity as an alpha-adrenergic blocking agent is most prominent during exercise. The full evaluation of prazosin-induced changes in the hemodynamics of patients of patients with chronic heart failure requires evaluation during exercise.
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PMID:Paradox of improved exercise but not resting hemodynamics with short-term prazosin in chronic heart failure. 42 18

The haemodynamic effects of oral prazosin and hydralazine were evaluated in patients with refractory heart failure and compared with those of intravenous nitroprusside in the same patients. Both oral agents were well tolerated and appeared to have beneficial haemodynamic effects. Prazosin and hydralazine produced similar increases in cardiac output associated with a similar decrease in systemic vascular resistance. Prazosin and hydralazine produced similar increases in cardiac output associated with a similar decrease in systemic vascular resistance. Prazosin resulted in a more significant decline in left ventricular filling pressure and pulmonary vascular resistance than did hydralazine. Haemodynamic alterations induced by prazosin were similar to those induced by nitroprusside, which suggests a relatively balanced reduction of preload and afterload. With hydralazine, the increase in cardiac output without change in left ventricular filling pressure or pulmonary vascular resistance suggests minimal effect on preload but significant reduction in afterload.
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PMID:Comparison of haemodynamic effects of oral prazosin, oral hydralazine, and intravenous nitroprusside in same patients with chronic heart failure. 53 83

Data are presented on 282 patients who began taking prazosin before March, 1975, and whose progress was followed until March, 1976. The following conclusions can be drawn. (i) Prazosin is an effective and useful antihypertensive agent, best used with a diuretic and a beta-blocker. (ii) For patients with suspected or definite coronary artery disease, prazosin should not be used without a beta-blocker. (iii) In patients suspected of having incipient heart failure, prazosin should not be used without a diuretic, and the latter should be given first. (iv) many patients have little or no rise in heart rate with prazosin. However, patients with sinus tachycardia or a history of arrhythmias should preferably not be treated with prazosin. (v) The initial dose should be kept small (0-25 to 0-5 mg). Subsequent increments should also be small, not more than 2 mg/day. (vi) If prazosin is added to a regimen containing an adrenergic neurone-blocking drug, the dose of the latter should first be reduced. (vii) Prazosin should not, in the meantime, be used concomitantly with a phenothiazine, as the combination appears to be capable of causing agitation and confusion. (viii) There seems to be no long-term toxicity.
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PMID:Initial experience with prazosin in New Zealand. A multicentre report. New Zealand Hypertension Study Group. 91 29

Postjunctional alpha-adrenoceptor characteristics were evaluated in canine dorsal pedal arterial and saphenous vein rings studied before and after development of severe pacing-induced heart failure (CHF). Before CHF, all agonists produced concentration-dependent increases in tension of both blood vessels. After development of CHF, the responsiveness and sensitivity of the vessels to the alpha 1-agonists and the mixed agonists were significantly increased as compared with control. The maximum responses to BHT 920 and BHT 933 remained unaltered after CHF, but both vessels showed decreased sensitivity to BHT 920. Before CHF, the rank order of potency with respect to norepinephrine (NE) for the dorsal pedal artery was as follows: NE greater than epinephrine greater than methoxamine greater than BHT 933 greater than BHT 920, and for the saphenous vein was epinephrine greater than NE greater than BHT 933 greater than methoxamine greater than BHT 920. At peak CHF, the rank order of potency for the artery was epinephrine greater than NE greater than methoxamine greater than BHT 933 greater than BHT 920, whereas in the vein BHT 920 was approximately 80 times less potent than NE (as compared with being only five times less potent before CHF). Prazosin was a potent, competitive antagonist (pA2 values of 9.2 and 9.0 for the artery and the vein) of methoxamine-induced contractions before development of CHF. Prazosin had a 10-fold lower potency against epinephrine-induced contractions in the dorsal pedal artery, whereas it was not competitive against epinephrine in the saphenous vein. Against the selective alpha 2-agonists, prazosin either showed no antagonism or was not competitive. After CHF, prazosin was non competitive against all agonists tested. Yohimbine was a potent, competitive antagonist against BHT 920 both before and at CHF. Yohimbine had intermediate antagonism against epinephrine and produced no antagonism of methoxamine-induced contractions. We conclude that increased reactivity and sensitivity of the peripheral vasculature to alpha 1-agonists occurs at CHF.
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PMID:Pacing-induced heart failure in the dog: evaluation of peripheral vascular alpha-adrenoceptor subtypes. 170 91

Competitive alpha1-adrenoceptor antagonists are effective in the treatment of both hypertension and cardiac failure. Prazosin has both a short half-life and a short duration of action, but other related quinazoline derivatives, such as doxazosin and terazosin, have pharmacokinetic and pharmacodynamic profiles which make them potentially suitable for once-daily administration. Acute reductions in blood pressure have been correlated with plasma concentrations of prazosin but in most instances, particularly during long term therapy, there is no simple, direct relationship between drug concentration and the fall in blood pressure. Using integrated pharmacokinetic-pharmacodynamic analysis, correlations have been described not only for reductions in blood pressure during short and long term treatment but also for alpha1-adrenoceptor antagonist activity. Furthermore, this integrated approach defines the drug concentration-effect relationship in individual subjects and provides a mathematical description of response that is potentially useful for investigating the factors (both kinetic and dynamic) which influence the inter- and intrasubject variability in antihypertensive effect of alpha-adrenergic blockers. Preliminary data suggest that the long term response to treatment with prazosin and doxazosin is mainly dependent upon the height of the pretreatment blood pressure and the response to the first dose.
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PMID:Pharmacokinetic-pharmacodynamic relationships of alpha-adrenoceptor antagonists. 257 89

Vasodilators may be required when signs of cardiac failure persist, despite adequate digitalo-diuretic therapy. Prazosin is a post-synaptic alpha-blocker which acts on both cardiac preload and afterload. For this reason, it has been widely used in the treatment of cardiac failure. We used prazosin in an open uncontrolled trial in 17 patients with an average of 59 years, in whom Stage III or IV cardiac failure persisted despite digitalis and diuretic therapy. Haemodynamic data obtained with a Swan Ganz catheter was used to judge the effectiveness of an initial dose of prazosin and long-term results were assessed by repeat studies after 6 and 10 weeks of continuous therapy. After the first, we observed a marked fall in pulmonary capillary (15.5% 7.4 vs 22.9% 8.8 mm Hg, p less than 0.01) and mean pulmonary artery pressures (23.8% 9.2 vs 34.2 +/- 10.6 mm Hg, p less than 0.001). Systemic vascular resistances were also significantly reduced (1 370 +/- 406 vs 1 983 +/- 464 dynes.s.cm-5, p less than 0.001). There was a moderate fall in mean systemic blood pressure (80.8% 10.6 vs 95.6 +/- 129 mm Hg, p less than 0.001). Cardiac index increased significantly (2.7 +/- 0.68 vs 2.13% 0.56 1/min/m2, p less than 0.01). The heart rate was constant. The maintenance dose was 5 mg three times daily in 9 cases, and 10 mg three times daily in the other 8 cases. The medium term results were assessed in 14 patients as 2 patients died and 1 stopped treatment for undetermined reasons. The symptomatic improvement was marked (class 2.5 +/- 0.76 vs 3.64 +/- 0.49, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prazosin in the treatment of chronic cardiac insufficiency]. 286 24

The effect of three months of prazosin treatment on the hemodynamics, cardiac extracellular space; plasma, tissue and intra-cellular Na+, K+, and Ca++ were investigated in dogs with left ventricular failure due to chronic mitral insufficiency. Mitral insufficiency of 6 months duration significantly decreased the LV systolic pressure, LV dp/dt, LV (dp/dt)/IIP, LVWI, CI, and increased the LVEDP, mean right atrial pressure, heart rate and systemic vascular resistance. Associated with these hemodynamic changes were an increase in the extra-cellular space, tissue and intracellular K+; and a decrease in the tissue and intracellular Ca++. Prazosin treatment produced an improvement in the hemodynamics which was associated with a decreased in the extracellular space, and intracellular K+, and an increase in the intracellular Ca++. Plasma Na+ and Ca++ increased with 6 months of M.I. Prazosin treatment brought back the plasma Na+ and K+ to control level. However, plasma Ca+ decreased significantly with prazosin treatment. The changes in right ventricular hemodynamics and electrolytes were not consistent with the right ventricular failure. These results indicate that decrease in the myocardial contractility in chronic heart failure due to mitral insufficiency might be due to a decrease in the intracellular Ca++. Prazosin treatment was able to reverse the hemodynamic and electrolyte changes induced by failing heart due to mitral insufficiency.
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PMID:Effect of chronic prazosin treatment on the cardiac function and electrolytes in failing heart due to chronic mitral insufficiency. 385 Jul 66

Prazosin is a selective alpha 1-adrenoceptor antagonist which is useful alone or in combination for the treatment of hypertension and heart failure. Unlike many other antihypertensive drugs, the action of prazosin appears to be closely related to its concentration in plasma or whole blood. Prazosin is variably absorbed, is subject to first-pass metabolism, and is eliminated almost entirely as metabolites of much lower hypotensive activity than the parent drug. Prazosin is highly bound to plasma and tissue proteins. The influences of renal, hepatic and cardiac disease on the disposition of prazosin are reviewed, as are the effects of pregnancy and ageing. The optimum use of prazosin in clinical practice depends on an understanding of the pharmacokinetic properties of the drug.
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PMID:Clinical pharmacokinetics of prazosin--1985. 388 89

During exercise in patients with heart failure, activation of sympathetic vasoconstrictor nerves may impair vasodilation in active skeletal muscle and thereby interfere with skeletal muscle blood flow. To investigate this hypothesis, we examined the effect of acute alpha-adrenergic blockade with systemic administration of prazosin (10 patients) or regional administration of phentolamine (eight patients) on blood flow, vascular resistance, oxygen consumption (VO2), and lactate release in the leg during maximal bicycle exercise in patients with heart failure. During control exercise, systemic VO2 increased to 12.6 +/- 4.3 ml/min/kg (normal greater than 20 to 25 ml/min/kg), leg blood flow to 2.8 +/- 1.8 liters/min, and leg lactate release to 362 +/- 256 mg/min. Prazosin decreased systemic vascular resistance (12.5 +/- 3.2 to 9.7 +/- 2.5 units; p less than .003) and mean arterial pressure (101 +/- 20 to 87 +/- 22 mm Hg; p less than .002) at maximal exercise, supporting the presence of substantial sympathetic vasoconstrictor nerve activity. Prazosin also decreased leg resistance during exercise. However, the magnitude of leg blood flow, leg oxygen extraction, and leg VO2 during exercise were unchanged, suggesting that vasodilation in the leg was produced by an autoregulatory response to the drop in blood pressure rather than by blockade of sympathetic vasoconstriction. Maximal systemic VO2 and leg lactate release were also not improved. Regional blockade with phentolamine did not substantially drop the arterial blood pressure and had no effect on vasodilation, blood flow, VO2, and lactate release in the leg during exercise. These data suggest that during exercise in patients with heart failure, the sympathetic nervous system helps to sustain arterial blood pressure and that this beneficial effect is not associated with adverse effects on blood flow to working skeletal muscle.
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PMID:Effect of the sympathetic nervous system on limb circulation and metabolism during exercise in patients with heart failure. 400 38


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