Catecholamine excretion and cardiac stores of norepinephrine in congestive heart failure

Chidsey, Charles A.; Braunwald, Eugene; Morrow, Andrew G.

doi:10.1016/0002-9343(65)90211-1

Cited by 551 publications

(126 citation statements)

References 22 publications

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“…13 [25][26][27][28][29] In either case, in patients with severe left ventricular failure, plasma catecholamines fail to increase and may even decrease with vasodilators;"'' 30 this is consistent with our observations that patients with a markedly reduced CI manifested little change or even decreases in HR despite significant decreases in systemic pressures during therapy and demonstrated mild rebound changes. Patients in our study with a mildly reduced CI, however, manifested reactions similar to those of normal and hypertensive subjects, which is consistent with experimental evidence that baroreceptor reflexes are only mildly attenuated in subjects in whom ventricular function is only mildly impaired.…”

Section: Discussionsupporting

confidence: 78%

Determinants of drug response in severe chronic heart failure. 1. Activation of vasoconstrictor forces during vasodilator therapy.

Packer¹,

Meller²,

Medina³

et al. 1981

Circulation

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SUMMARY Vasodilator drugs activate neurohumoral forces that produce peripheral vasoconstriction and tachycardia and probably cause the rebound events observed upon abrupt withdrawal of therapy. To determine their role in limiting therapeutic vasodilator responses, these reactive forces were measured in 40 patients with severe chronic heart failure by quantifying the magnitude of rebound change (MRC) after nitroprusside withdrawal. Group 1 patients (n = 22), who had minimal reactive vasoconstriction (MRC 27%), showed marked hemodynamic effects with nitroprusside (4.5 ,g/kg/min) and isosorbide dinitrate (40 mg orally), associated with significant decreases in heart rate with both drugs (p < 0.001). Despite administration of the same doses of both drugs, group 2 patients (n = 18), who had marked rebound changes (MRC > 27%), showed significantly smaller changes in cardiac index, systemic vascular resistance and mean arterial pressure (p < 0.001), associated with no change or increases in heart rate. Rebound events were attenuated and the responses to nitroprusside and nitrates were enhanced in four patients in whom these drugs were readministered after pretreatment with i.v. phentolamine (0.3 mg/min). We conclude that activation of neurohumoral forces can limit the hemodynamic responses to vasodilator administration; this supports the use of combination therapy of direct-acting vasodilators and neurohumoral antagonists in selected patients with severe chronic heart failure.

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Section: Discussionsupporting

confidence: 78%

Determinants of drug response in severe chronic heart failure. 1. Activation of vasoconstrictor forces during vasodilator therapy.

Packer¹,

Meller²,

Medina³

et al. 1981

Circulation

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“…[22][23][24] In contrast, it has been shown that in patients with ischemic heart disease, f8-blockers may improve the left ventricular function by balancing the oxygen needs of the jeopardized myocardium.0' 11,25 Whether or not the development of congestive heart failure in postinfarction patients is caused by reinfarction or by loss of compensatory sympathetic support is not known at the present time.…”

Section: Discussionmentioning

confidence: 96%

Effect of propranolol after acute myocardial infarction in patients with congestive heart failure.

Chadda¹,

Goldstein²,

Byington³

et al. 1986

Circulation

371

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The incidence of congestive heart failure was studied in the Beta Blocker Heart Attack Trial in which postmyocardial infarction patients between the ages of 30 and 69 years, with no contraindication to propranolol, were randomly assigned to receive placebo (n = 1921) or propranolol 180 or 240 mg daily (n = 1916) 5 to 21 days after admission to the hospital for the event. Survivors of acute myocardial infarction with compensated or mild congestive heart failure, including those on digitalis and diuretics, were included in the study. A history of congestive heart failure before randomization characterized 710 (18.5%) patients: 345 (18.0%) in the propranolol group and 365 (19.0%) in the placebo group. The incidence of definite congestive heart failure after randomization and during the study was 6.7% in both groups. In patients with a history of congestive heart failure before randomization, 51 of 345 (14.8%) in the propranolol group and 46 of 365 (12.6%) in the placebo group developed congestive heart failure during an average 25 month follow-up. In the patients with no history of congestive heart failure, 5% in the propranolol group developed congestive heart failure and 5.3% in the placebo group developed congestive heart failure. Baseline characteristics predictive of the occurrence of congestive heart failure by multivariate analyses included an increased cardiothoracic ratio, diabetes, increased heart rate, low baseline weight, prior myocardial infarction, age, and more than 10 ventricular premature beats per hour. Patients with congestive heart failure in the propranolol group experienced a similar decrease in the total mortality (27%) compared with those without congestive heart failure (25%), whereas propranolol decreased the occurrence of sudden death by 47% in the patients with prior heart failure compared with 13% without congestive heart failure. Circulation 73, No. 3, 503-510, 1986. THE USE OF ,3-adrenergic blocking agents in survivors of acute myocardial infarction with evidence of congestive heart failure poses a therapeutic paradox for the clinician. A number of 3-adrenergic blocking agents have been shown to decrease the mortality rate in postmyocardial infarction patients when administered between 1 and 3 weeks after the event. 1-' Patients with evidence of severe heart failure were usually but not always excluded from enrollment in these studies. These reports have been supplemented by both prospective and retrospective studies suggesting that a relatively greater benefit, including a significant reduction in sudden death, may be realized in the group of patients at the highest risk of future events. The Beta Blocker Heart Attack Trial (BHAT) offers an opportunity to evaluate the effect of long-term therapy with propranolol in patients after an acute myocardial infarction with congestive heart failure. As part of the design and safety features, patients with shock or overt heart failure were excluded from enrollment in BHAT until these conditions were ameliorated. In this analysis we wi...

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“…The combination of myocardial support and peripheral vasodilatation is particularly appealing in this regard. The agent may also find use as a substitute for indirect acting sympathomimetic amines, such as mephentermine, in those patients with depleted myocardial catecholamines (Chidsey, Braunwald & Morrow, 1965). In this latter regard MJ-1988 is not subject to inactivation in the acidotic state which is a problem with the catecholamines (Aviado, 1965 Compound MJ-1988 (6,7-dimethoxy-4-ethylquinazoline) was infused into normal and cardiac denervated dogs, at the rate of 0.375 mg/kg/min, while on a right heart bypass which permitted control of heart rate, cardiac input and arterial blood pressure.…”

Section: Discussionmentioning

confidence: 99%

Effects of Compound Mj‐1988 on Myocardial Contractility, Oxygen Consumption, Coronary Blood Flow and Vascular Resistance

Carr

Cooper

Daggett

et al. 1967

British Journal of Pharmacology and Chemotherapy

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Preliminary reports have shown that 6,7-dimethoxy-4-ethylquinazoline, known as MJ-1988, possesses potent cardiac stimulating, bronchodilator and vasodilating properties (Lish, Cox, Dungan & Robbins, 1964). A drug with this combination of pharmacological effects might have important therapeutic possibilities. This study was undertaken to assess the potency of an effective dose of .the compound on the contractility of the working canine left ventricle. The experimental preparation used also allowed the assessment of coronary blood flow, myocardial oxygen consumption and vascular resistance. METHODSExperiments were performed in adult mongrel dogs, weighing 10.5 to 17 kg. The dogs were anaesthetized by an intravenous infusion of a warmed solution of urethane (600 mg/kg) and chloralose (60 mg/kg). The rate and depth of respiration was controlled by a Bird Mark 8 positive pressure respirator. The chest was opened through a median sternotomy and the working left heart model was prepared as follows (Fig. 1). After preliminary dissection, haemostasis, and isolation of a femoral artery, heparin, 3 mg/kg, was administered, followed by 30 mg every hour. The superior and inferior vena cavae were cannulated and the azygos vein divided. The caval return was led to a reservoir (Res. 1) by siphon drainage. From the reservoir the blood drained by gravity to a bubble oxygenator. Oxygenated blood, warmed to 370 C, was returned via a roller pump (P) through a Shipley-Wilson rotameter (RI) to the main pulmonary artery. A ligature placed around the cannulated pulmonary artery thus completely isolated the right heart so that it received only coronary venous drainage. The total coronary flow (less left ventricular Thebesian flow) was led from the cannulated right heart through a rotameter (R2) to the reservoir (Res. 1). This rotameter was calibrated during each experiment by timed volumetric collection of coronary venous blood flow.

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Catecholamine excretion and cardiac stores of norepinephrine in congestive heart failure

Cited by 551 publications

References 22 publications

Determinants of drug response in severe chronic heart failure. 1. Activation of vasoconstrictor forces during vasodilator therapy.

Determinants of drug response in severe chronic heart failure. 1. Activation of vasoconstrictor forces during vasodilator therapy.

Effect of propranolol after acute myocardial infarction in patients with congestive heart failure.

Effects of Compound Mj‐1988 on Myocardial Contractility, Oxygen Consumption, Coronary Blood Flow and Vascular Resistance

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