Methodological Considerations in the Determination of Plasma Catecholamines by High-Performance Liquid Chromatography with Electrochemical Detection

Bouloux, Pierre; Perrett, David; Besser, G. M.

doi:10.1177/000456328502200217

Cited by 150 publications

(53 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Norepinephrine and epinephrine levels were measured in EDTA plasma using high-performance liquid chromatography with electrochemical detection, as previously described. 23 For all subjects, the full blood count, renal function, and liver function were determined using routine laboratory methods.…”

Section: Neurohormone Assessmentmentioning

confidence: 99%

Neurohormonal Activation and the Chronic Heart Failure Syndrome in Adults With Congenital Heart Disease

et al. 2002

View full text Add to dashboard Cite

Background — Neurohormonal activation characterizes chronic heart failure, relates to outcome, and is a therapeutic target. It is not known whether a similar pattern of neurohormonal activation exists in adults with congenital heart disease and, if so, whether it relates to common measures of disease severity or whether cardiac anatomy is a better discriminant. Methods and Results — Concentrations of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), endothelin-1 (ET-1), renin, aldosterone, norepinephrine, and epinephrine were determined in 53 adults with congenital heart disease, comprising 4 distinct anatomic subgroups (29 female; 33.5±1.5 years of age; New York Heart Association class 2.0±0.1, mean±SEM) and 15 healthy control subjects (8 female; 32.3±1.3 years of age). Systemic ventricular function was graded by a blinded echocardiographer as normal or mildly, moderately, or severely impaired. Adults with congenital heart disease had elevated levels of ANP (56.6 versus 3.1 pmol/L), BNP (35.8 versus 5.7 pmol/L), ET-1 (2.5 versus 0.7 pmol/L, all P <0.0001), renin (147 versus 16.3 pmol/L), norepinephrine (2.2 versus 1.6 pmol/L, both P <0.01) and aldosterone (546 versus 337 pmol/L, P <0.05). There was a highly significant stepwise increase in ANP, BNP, ET-1, and norepinephrine according to New York Heart Association class and systemic ventricular function, with even asymptomatic patients having evidence of significant neurohormonal activation. In contrast, there was no direct relationship between the 4 anatomic subgroups and any of the neurohormones studied. Conclusions — Neurohormonal activation in adult congenital heart disease bears the hallmarks of chronic heart failure, relating to symptom severity and ventricular dysfunction and not necessarily to anatomic substrate. Neurohormonal antagonism across this large and anatomically diverse population should be considered.

show abstract

Section: Neurohormone Assessmentmentioning

confidence: 99%

Neurohormonal Activation and the Chronic Heart Failure Syndrome in Adults With Congenital Heart Disease

et al. 2002

View full text Add to dashboard Cite

show abstract

“…After the transmission scan, radioactive gases were delivered at a constant rate by a standard facemask used clinically for delivering oxygen (MC oxygen mask, Henlys Medical). A blood pool scan was performed by inhalation of 15 Olabeled carbon monoxide (C 15 O), delivered at a rate of 500 mL/min, with 3 MBq/mL activity for 4 minutes. The inhaled C 15 …”

Section: Positron Emission Tomographymentioning

confidence: 99%

“…Redistribution of myocardial blood flow from regions supplied by a severely stenosed coronary artery to those supplied by less diseased, or normal vessels, might offer an explanation for postprandial angina. To test this hypothesis, we have determined the effects of a standard liquid meal on whole heart and regional myocardial blood flow by using positron emission tomography (PET) with 15 O-labeled water in patients with a reproducible history of postprandial angina.…”

mentioning

confidence: 99%

Regional Myocardial Blood Flow Redistribution as a Cause of Postprandial Angina Pectoris

et al. 1998

View full text Add to dashboard Cite

Background-Postprandial angina pectoris has been recognized for more than two centuries and can be identified in up to 10% of patients with chronic ischemic heart disease. Redistribution of myocardial blood flow, from a region supplied by a severely stenotic coronary artery to those supplied by less diseased or normal vessels, is a potential mechanism of postprandial angina. Methods and Results-To test this hypothesis, we have determined the effects of a standard liquid meal on whole heart and regional myocardial blood flow, measured by means of dynamic positron emission tomography (PET) with

show abstract

“…Interassay coefficient of variation = 2.5% Plasma NE, E, and Dopamine (DA)-NE, E, and DA were determined by HPLC with dihydroxybenzylamine as the internal standard using a modification of the method of Bouloux et al (1985). Free NE, E, and DA were determined quantitatively using a dual electrode electrochemical detector.…”

Section: Biochemical Methodsmentioning

confidence: 99%

Enhanced norepinephrine output during long-term desipramine treatment: A possible role for the extraneuronal monoamine transporter (SLC22A3)

Mooney

Samson

Hennen

et al. 2008

Journal of Psychiatric Research

View full text Add to dashboard Cite

To study the delay (2-6 weeks) between initial administration of norepinephrine reuptake inhibitor antidepressants and onset of clinical antidepressant action, we examined the effects of desipramine treatment on urinary and plasma catecholamines and their metabolites during the initial 6 weeks of treatment in depressed patients. Catecholamines and metabolites in 24-hour urine collections and 8:00 a.m. plasma samples were measured at baseline and after 1, 4, and 6 weeks of desipramine treatment. Desipramine treatment produced significant increases in urinary norepinephrine (NE) and normetanephrine (NMN) and plasma NE at Weeks 4 and 6, but not at Week 1. The ratio of urinary NE/NMN was increased at Weeks 4 and 6, suggesting a reduction in the metabolism of NE to NMN at extraneuronal sites by Weeks 4 and 6. The increases in urinary NE and NMN and plasma NE at Weeks 4 and 6 of desipramine treatment were associated with a reduction in the conversion of NE to NMN. This would be compatible with a blockade of the extraneuronal monoamine transporter (organic cation transporter 3; SLC22A3) by NMN. Inhibition of the extraneuronal monoamine transporter may be an important component in the clinical pharmacology of the norepinephrine reuptake inhibitor antidepressant drugs, such as desipramine. The ClinicalTrials.gov Identifier for this study is NCT00320632.

show abstract

Methodological Considerations in the Determination of Plasma Catecholamines by High-Performance Liquid Chromatography with Electrochemical Detection

Cited by 150 publications

References 30 publications

Neurohormonal Activation and the Chronic Heart Failure Syndrome in Adults With Congenital Heart Disease

Neurohormonal Activation and the Chronic Heart Failure Syndrome in Adults With Congenital Heart Disease

Regional Myocardial Blood Flow Redistribution as a Cause of Postprandial Angina Pectoris

Enhanced norepinephrine output during long-term desipramine treatment: A possible role for the extraneuronal monoamine transporter (SLC22A3)

Contact Info

Product

Resources

About