An Improved Method for Fluorimetric Determination of Small Amounts of Adrenaline and Noradrenaline in Plasma and Tissues

Häggendal, Jan

doi:10.1111/j.1748-1716.1963.tb02739.x

Cited by 522 publications

(79 citation statements)

References 13 publications

(2 reference statements)

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“…After thawing and centrifugation of the homogenate, brain noradrenaline and dopamine were isolated according to the procedure of Anton & Sayre (1962). Noradrenaline was assayed according to the method of Haggendal (1963); dopamine according to the method of Anton & Sayre (1964).…”

Section: Methodsmentioning

confidence: 99%

Depletion of brain noradrenaline and dopamine by 6‐hydroxydopamine

Breese¹,

Traylor²

1971

British J Pharmacology

527

135

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Summary1. After intracisternal administration, 6-hydroxydopamine had a greater effect on brain noradrenaline than on dopamine. 2. Administration of two doses of 6-hydroxydopamine increased the depletion of noradrenaline but not of dopamine.3. Small doses of 6-hydroxydopamine decreased the concentration of noradrenaline with little or no effect on dopamine. Tyrosine hydroxylase activity was not reduced with these treatments.4. While pargyline pretreatment offered no advantage in the depletion of brain noradrenaline after 6-hydroxydopamine, depletion of brain dopamine was greatly potentiated by this treatment. The reduction of striatal tyrosine hydroxylase activity observed after 6-hydroxydopamine was also potentiated by pargyline pretreatment. 5. The amounts of labelled noradrenaline and dopamine formed from 3H-tyrosine were greatly reduced by 6-hydroxydopamine treatment. After 3H-DOPA, formation of noradrenaline was greatly reduced while formation of labelled dopamine was only moderately reduced suggesting that decarboxylation of DOPA can occur in other than catecholamine containing neurones. 6. Desmethylimipramine and imipramine inhibited depletion of noradrenaline produced by 6-hydroxydopamine but did not alter depletion of dopamine.Reserpine did not inhibit depletion of catecholamines produced by 6-hydroxydopamine. 7. Administration of 6-hydroxydopamine to developing rats lowered both noradrenaline and dopamine concentrations as well as the tyrosine hydroxylase activity in the brains of these animals.

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Section: Methodsmentioning

confidence: 99%

Depletion of brain noradrenaline and dopamine by 6‐hydroxydopamine

Breese¹,

Traylor²

1971

British J Pharmacology

527

135

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“…Haggendal, 1963), can only occur after acidification. This ' development ' can then be accelerated by the introduction of energy, but the chemical changes involved are unknown.…”

Section: Discussionmentioning

confidence: 99%

The determination of dopamine by a modification of the dihydroxyindole fluorimetric assay

Atack

1973

British J Pharmacology

249

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Summary1. A simplified sensitive fluorimetric assay for dopamine based on the hydroxyindole principle is described. Oxidation of dopamine by ferricyanide and subsequent tautomerization both occur in the same, strongly alkaline, ethanolic solution in the presence of metabisulphite. The reaction is selfregulating, and since times of additions of reagents are relatively unimportant and the final fluorescence is very stable, a large number of samples can be assayed together.2. The method was developed for assaying dopamine in N-ethanolic (50%)-HCI eluates, after purification on a strongly acidic cation exchange column as previously described (Atack & Magnusson, 1970). Portions, up to 1 ml volume, of the 3 5 ml eluate can be taken. No preliminary, time-consuming, neutralization step is required before oxidation. Fluorescence intensity shows a linear re!ation with concentration for 1-5,000 ng of dopamine per 1-6 ml of final solution, both in pure solutions and in column eluates. 3. Fluorescence readings from biological material are given, with evidence for their reproducibility. These, together with other data, demonstrate the relative accuracy of the 'tissue blank' and indicate that amounts of dopamine greater than 3 ng per column can confidently be detected, and amounts greater than 10 ng can be measured quantitatively. 4. Fluorescence spectra are presented for the fluorophore derived from authentic dopamine, and from suspected dopamine extracted from spinal cord of normal rats and rats treated with reserpine plus an inhibitor of synthesis.Values for the concentration of dopamine of 20 and <3 ng/g, respectively, were obtained.

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“…Plasma epinephrine and 1-norepinephrine contents were measured by a modified method of Huggendal (26), using dithiothreitol instead of demarcaptopropanol as a stabilizer for lutine fluorescence. The coefficient of variation averaged 9.15 and 9.66% (n = 28) for epinephrine and 1-norepinephrine, respectively.…”

Section: Methods Of Analysismentioning

confidence: 99%

Propranolol during the evolution and subsequent ten days of myocardial infarction in man: Hemodynamic, initial cardiac energetic, and neurohumoral responses

Müeller

Rao

Fletcher

et al. 1979

Clinical Cardiology

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Summary: During the evolution of transmural myocardial infarction an intensive sympathetic hyperactivity was observed. Plasma I-norepinephrine and epinephrine contents were strikingly increased, the mean values to 2.04fl .I0 (SD) and 0.94f0.48 pg/l, respectively. Propranolol(O.1 mg/kg) was administered intravenously within an average of 8.8 h of transmural myocardial infarction to 55 patients who did not show significant left ventricular failure. The drug was continued orally with an average dose of 56f20 (SD) mg q6h for 10 d. Mean plasma propranolol levels during the first 5 d ranged between 89 and 162 ng/ml. Cardiac index, left ventricular ejection fraction, and, to a lesser degree, blood pressure significantly decreased. Mean pulmonary capillary wedge pressure remained unchanged. Decreases in coronary blood flow and myocardial oxygen consumption were associated with improvement of myocardial lactate metabolism, suggesting reduced myocardial oxygen requirements. Plasma free fatty acid contents significantly decreased. Myocardial glucose extraction and respiratory quotient increased, indicating enhanced carbohydrate utilization. Prior to propranolol administration, plasma glucose and glucagon contents were increased and plasma insulin levels were inappropriately low. Initial glucagon and initial I-norepinephrine and epinephrine contents were correlated (r = 0.54 and 0.50, p <0.01). Beta-adrenergic blockade decreased plasma insulin contents in spite of hyperglycemia and abolished the correlation between glucagon and catecholamines. Propranolol was tolerated well by all patients; none of them developed acute left ventricular failure.The study demonstrates that propranolol can be safely administered during the evolution and early phase of transmural myocardial infarction, if selection criteria for patients are carefully considered. Propranolol, dampening the response to acute ischemic stress, diminishes energy requirements and thus appears to be a promising drug for preservation of ischemic myocardium.

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An Improved Method for Fluorimetric Determination of Small Amounts of Adrenaline and Noradrenaline in Plasma and Tissues

Cited by 522 publications

References 13 publications

Depletion of brain noradrenaline and dopamine by 6‐hydroxydopamine

Depletion of brain noradrenaline and dopamine by 6‐hydroxydopamine

The determination of dopamine by a modification of the dihydroxyindole fluorimetric assay

Propranolol during the evolution and subsequent ten days of myocardial infarction in man: Hemodynamic, initial cardiac energetic, and neurohumoral responses

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