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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Simultaneous hemodynamic and radionuclide angiographic assessment was made at rest and during exercise in nine patients with severe chronic congestive heart failure to determine the value of radionuclide left ventricular ejection fraction measurement in predicting the hemodynamic response to short-term treatment with oral hydralazine. Hydralazine, 50 to 100 mg orally every 6 hours, produced significant increases in cardiac index and stroke volume index at rest and during exercise (p less than 0.01) and in left ventricular stroke work index at rest (p less than 0.01) and during exercise (p less than 0.05), significant decreases in systemic vascular resistance at rest and during exercise (p less than 0.01) and significant increases in radionuclide angiographic left ventricular ejection fraction at rest (control 0.21 +/- 0.06 vs. hydralazine 0.26 +/- 0.07, p less than 0.01) and during exercise (control 0.21 +/- 0.08 vs. hydralazine 0.24 +/- 0.09, p less than 0.05). However, there were no statistically significant correlations between changes in radionuclide ejection fraction with hydralazine and changes in hemodynamic variables with hydralazine, either at rest or during exercise. Patients responding hemodynamically to hydralazine could not be separated from those not responding on the basis of the radionuclide ejection fraction at rest or changes in ejection fraction with hydralazine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hydralazine therapy in severe chronic heart failure: inability of radionuclide left ventricular ejection fraction measurement to predict the hemodynamic response. 631 88

The acute effects of intravenously administered hydralazine on pulmonary hemodynamics and ejection radionuclide angiography were evaluated in 9 patients with chronic airflow obstruction (forced expiratory volume in one second, 1.2 +/- 0.8 L, mean +/- SD), pulmonary hypertension (mean pulmonary artery pressure (PAP), 29 +/- 13 mmHg), and sleep hypoxemia (maximal sleep desaturation, 20 +/- 16%). The effect of hydralazine was measured during both normoxia and hypoxia and compared with the effect of hyperoxia. Hydralazine increased cardiac index from 3.7 +/- 0.2 to 4.5 +/- 0.8 L/min/m2 (mean +/- SE, p less than 0.05, n = 9), but there were no significant changes in PAP (29 +/- 4 to 32 +/- 4 mmHg), mean pulmonary vascular resistance index (PVRI) (390 +/- 80 to 360 +/- 80 dyn.s.cm.-5.m2), mean right ventricular stroke work index (12.7 +/- 2.7 to 15.0 +/- 2.2 g.m/m2), and mean pulmonary capillary wedge pressure (12 +/- 1 to 12 +/- 2 mmHg). Mean right ventricular ejection fraction and mean right ventricular end diastolic volume also were not changed after treatment with hydralazine. Hyperoxia was used to assess the reversibility of pulmonary hypertension and to compare this with hydralazine. Hyperoxia increased arterial oxygen saturation (SaO2) from 91 +/- 1 to 96 +/- 1% and decreased the cardiac index from 3.8 +/- 0.1 to 3.1 +/- 0.2 L/min/m2 (p less than 0.02, n = 6) but, as with hydralazine, there was no significant change in PAP (28 +/- 6 to 25 +/- 6 mmHg) and PVRI (350 +/- 120 to 360 +/- 80 dyn.s.cm-5).m2).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Detrimental effects of hydralazine in patients with chronic air-flow obstruction and pulmonary hypertension. A combined hemodynamic and radionuclide study. 632 27

Hydralazine is a smooth muscle relaxant and a potent arteriolar dilator. The major hemodynamic effect of hydralazine in patients with heart failure are increased cardiac output and stroke volume, and decreased vascular resistance without any significant change in pulmonary and systemic venous pressure. Hydralazine also produces beneficial hemodynamic effects in patients with mitral and aortic regurgitation and in some patients with large ventricular septal effect with reduced systemic output. However, the role of long-term hydralazine therapy in these patients remains uncertain. In many patients with chronic heart failure with low cardiac output, hydralazine produces sustained beneficial hemodynamic and clinical effects. The long-term prognosis of patients with chronic heart failure, however, remains unchanged, although certain subsets of patients appear to have better prognoses than others during long-term hydralazine therapy.
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PMID:Hydralazine in heart failure. 641 40

The pharmacodynamics of hydralazine, an arteriolar dilator, were studied in dogs with induced heart failure. The dogs were studied 5 days after heart failure was induced by injecting microspheres into the left circumflex coronary artery. All dogs had a stroke volume index less than 25 ml/beat/m2 of body surface and a left ventricular filling pressure greater than or equal to 16 mm of Hg. Approximately 1 mg of hydralazine/kg of body weight was administered orally each hour until the total systemic resistance index decreased below 1,700 dynes . s X cm-5 X m2. The drug effect was monitored hemodynamically until it dissipated. Hydralazine increased the cardiac index from 3.06 +/- 0.47 (+/- SD) to 6.81 +/- 0.87 L/min/m2 (P less than 0.01), stroke volume index from 20.9 +/- 1.6 to 36.8 +/- 9.3 ml/beat/m2 (P less than 0.01), and heart rate from 146.2 +/- 17.2 to 187.8 +/- 42.8 beats/min (P less than 0.05). It decreased mean arterial pressure from 111.5 +/- 20.4 to 83.8 +/- 4.7 mm of Hg (P less than 0.05) and total systemic resistance index from 2,903 +/- 149 to 992 +/- 83 dynes . s X cm-5 X m2 (P less than 0.001). It did not affect left ventricular filling pressure or contractility. Peak drug effect occurred at 3 to 5 hours after drug administration and duration of effect was 11 to 13 hours. Recurrence of ventricular dysrhythmias occurred in 2 dogs and 1 dog died during a recurrence. Hydralazine improved cardiac performance in the dog with left ventricular failure.
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PMID:Hydralazine pharmacodynamics in the dog. 662 99

The effects of 3 types of vasoactive agents, hydralazine, nifedipine and amrinone, were evaluated in 7 patients with primary pulmonary hypertension (PPH). Hemodynamic values were measured before and after drug administration in every patient. All drugs increased cardiac output and reduced both systemic and pulmonary resistance in the patients studied. Only nifedipine significantly reduced pulmonary artery (PA) pressure (6 +/- 5 mm Hg). In addition, it decreased pulmonary resistance to a greater degree than systemic resistance in 2 of the 7 patients, suggesting that nifedipine can cause selective pulmonary vasodilation in some patients. Hydralazine appeared to increase cardiac output and stroke volume by reducing systemic resistance. There was no evidence of direct pulmonary vasodilating effects; it decreased systemic resistance more than pulmonary resistance in every case. The increase in cardiac output from amrinone was secondary to a decrease in systemic arterial pressure with reflex tachycardia; stroke volume was unchanged. Amrinone had little pulmonary effect in all but 1 patient, in whom it substantially reduced PA pressure and pulmonary resistance. The mechanism of action of these 3 drugs in PPH differs. Nifedipine holds the most promise as an effective pulmonary vasodilator. A study of the effects of long-term administration of nifedipine in PPH is warranted.
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PMID:Comparative actions of hydralazine, nifedipine and amrinone in primary pulmonary hypertension. 663 31

The effect of afterload reduction was studied in a group of patients who remained breathless or tired after permanent ventricular pacing. Haemodynamic measurements were made before and after giving hydralazine 20 mg intravenously using a triple lumen thermodilution catheter and cuff blood pressure recordings during ventricular pacing at the standard rate of 71/min or an increased rate of 88/min and physiological pacing. Increasing the ventricular pacing rate had no effect on cardiac output as stroke volume fell. Hydralazine produced a greater rise in cardiac output than physiological pacing alone, although peak values were obtained by combining the two. Ventricular pacing produced intermittent large left and right atrial pressure peaks. Physiological pacing produced no such peaks, and mean right and left atrial pressures fell. Hydralazine did not significantly alter atrial pressures. These findings show that in these patients, most of whom had a low cardiac output, afterload reduction with ventricular pacing increased resting cardiac output more than physiological pacing alone. Nevertheless, persistence of high filling pressures despite afterload reduction may limit the potential therapeutic benefit. Care should be taken in extrapolating these data to other patient groups.
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PMID:Effect of afterload reduction in patients with ventricular and physiological pacing. 669 7

Using the radioactive microsphere technique, we investigated the interaction between atenolol and hydralazine after acute administration in conscious hypertensive rabbits. Hydralazine, 0.3 mg/kg i.v., increased heart rate, stroke volume and cardiac output and decreased total peripheral resistance. Only at higher doses (1.0 and 3.0 mg/kg i.v.) was a fall in arterial blood pressure observed due to a further reduction in total peripheral resistance. The drug caused vasodilatation in the heart, brain, kidneys, skeletal muscles, diaphragm, chest wall and large intestine and a, probably reflex-mediated, vasoconstriction in the skin, stomach and small intestine. In the heart hydralazine preferentially increased blood flow to the outer layers of the left ventricular wall, which resulted in a significant decrease in the endocardial/epicardial blood flow ratio. Hydralazine also greatly enhanced the percentage of 15-micron microspheres distributed to the lungs, indicating an increased arteriovenous anastomotic flow. Atenolol (1 mg/kg i.v.) elicited bradycardia and moderately reduced blood pressure due to a decrease in cardiac output. Pretreatment with atenolol attenuated the cardiac stimulation and thereby accentuated the hypotensive effect of hydralazine, 0.3 mg/kg. With the high hydralazine dose (3.0 mg/kg) the synergistic effect on blood pressure disappeared due to an increase in cardiac output, despite effective beta adrenoceptor blockade. Moreover, atenolol interfered with the vasodilator response of hydralazine in the heart, skeletal muscles and the arteriovenous anastomoses. The beta adrenoceptor antagonist increased the endocardial/epicardial blood flow ratio and thereby abolished the negative effect of hydralazine on this parameter. In conclusion, the antihypertensive drugs acted synergistically only at a low hydralazine dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interaction of atenolol with the systemic and regional hemodynamic effects of hydralazine in conscious renal hypertensive rabbits. 674 26

Coronary blood flow and myocardial energetics were assessed after the administration of a parenteral inotrope (dobutamine hydrochloride) and an oral vasodilator agent (hydralazine) in 10 patients with nonischemic congestive heart failure. Dobutamine (5 micrograms/kg per min) and hydralazine (1 mg/kg) when group-matched elicited an identical increase in cardiac index and stroke volume index. Both agents augmented coronary blood flow while reducing coronary vascular resistance. Both forms of therapy elicited a significant increase in myocardial oxygen consumption. Dobutamine, demonstrating a balanced effect on the coronary circulation, induced a proportional increase in coronary blood flow and myocardial oxygen consumption, with the arterial-venous oxygen difference across the coronary vascular bed remaining unchanged. Hydralazine enhanced the myocardial oxygen supply versus demand ratio; despite a significant increase in myocardial oxygen consumption, the arterial-venous oxygen difference and the myocardial extraction ratio diminished. Both forms of therapy enhanced cardiac performance without inducing any electrocardiographic or clinical evidence of ischemia. Dobutamine, a positive inotropic agent, elicited a balanced effect on the coronary circulation while hydralazine, a vasodilator agent, induced a greater increase in coronary flow than in myocardial oxygen demand.
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PMID:Dobutamine and hydralazine: comparative influences of positive inotropy and vasodilation on coronary blood flow and myocardial energetics in nonischemic congestive heart failure. 682 60

Despite the beneficial therapeutic effects of antihypertensive drugs, some agents--particularly diuretics--seem to go in the "wrong direction" chemically. In fact, these changes could counteract some of the benefits resulting from lowering a patient's blood pressure. In the absence of hard evidence of the efficacy of long-term diuretic treatment of mild hypertension, we must be maximally sure that such therapy causes no harm. Thiazide and related diuretics have been associated with four distinct wrong-way chemical changes: increases in plasma concentrations of cholesterol, glucose, and uric acid, and a decrease in plasma potassium levels. The potential ramifications of such changes are well understood. The increase in circulating cholesterol, an established risk factor of myocardial infarction and stroke, is of particular concern--each year approximately one million hypertensive patients have myocardial infarctions. As a result, the search for safer and more effective diuretics must continue. Indapamide, a new antihypertensive drug, appears to meet these criteria. It is an effective diuretic with a considerable peripheral vasodilatory effect. Additionally, it does not appear to induce any significant change in circulating cholesterol, whereas chlorthalidone has been found to increase total cholesterol by 5%. Hydralazine is the only antihypertensive agent that seems to lower total cholesterol levels significantly. Neither indapamide nor hydralazine appears to affect plasma glucose levels; benzothiadiazines, however, have been found to induce an increase in circulating glucose.
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PMID:Some wrong-way chemical changes during antihypertensive treatment: comparison of indapamide and related agents. 686 7

To determine whether the circulatory response to hydralazine in heart failure is influenced by initial hemodynamic status or left ventricular (LV) chamber size, 28 patients with chronic LV dysfunction were studied. Hemodynamic measurements and echocardiographic LV end-diastolic dimension were correlated with the response to 20 mg of intravenous hydralazine and to a dose titrated in each patient to reduce systemic resistance by greater than or equal to 20%. Hydralazine, 20 mg, decreased systemic resistance from 23 +/- 8 to 18 +/- 8 U (p less than 0.01) and increased the cardiac index from 2.0 +/- 0.5 to 2.5 +/- 0.6 liters/min/m2 (p less than 0.01) and the stroke work index from 21 +/- 11 to 24 +/- 9 g . m/m2 (p less than 0.05). Titrating the dose to decrease systemic resistance by greater than or equal to 20% increased the cardiac index further to 2.7 +/- 0.6 liters/min/m2 and the stroke work index to 32 +/- 9 g . m/m2. The change in systemic resistance produced by 20 mg of hydralazine correlated only with initial systemic resistance (r = 0.53), suggesting that vascular response to hydralazine is a direct function of initial vascular resistance. The percentage change in stroke work index produced by 20 mg of hydralazine correlated directly with indexes of LV preload-end-diastolic wall stress (r = 0.69) and pulmonary wedge pressure (r = 0.43) and inversely with stroke work index (r = -0.49), an index of ventricular work. Similar but less close correlations were observed when the dose of hydralazine was titrated. The hemodynamic response to hydralazine did not correlate with LV end-diastolic dimension or right atrial pressure. Thus, vascular response to moderate doses of hydralazine is related to initial systemic vascular resistance. LV pump response is related to the level of initial LV pump dysfunction but not to LV chamber size or right atrial pressure.
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PMID:Determinants of circulatory response to intravenous hydralazine in congestive heart failure. 686 77


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