The fate of 5-hydroxytryptamine in the lungs

Gruby, Lesley A.; Rowlands, C.A.; Varley, B. Q.; Wyllie, J. H.

doi:10.1002/bjs.1800580716

Cited by 28 publications

(13 citation statements)

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“…Although our work demonstrates conclusively the existence in man of 5-HT and NE inactivation by the lung, the physiological or pathophysiological significance of the inactivation is unknown despite earlier speculation (8,(10)(11)(12). Equally unclear is the effect of increased removal of these amines, particularly in the case of NE, after total cardiopulmonary bypass.…”

Section: Amine Removal By Human Lungmentioning

confidence: 50%

“…• Both 5-hydroxytryptamine (5-HT) and norepinephrine (NE) are removed, to varying degrees, from the pulmonary vascular space of dog (1-4), cat (5), rat (6,7), guinea pig (8), and rabbit (9). Pulmonary venous and, thus, systemic arterial blood concentrations of these amines are significantly decreased by passage through the lung.…”

mentioning

confidence: 99%

“…However, if lung rather than liver is the major site of 5-HT inactivation (10), then these symptoms may likewise reflect inefficiency of pulmonary mechanisms for removal of 5-HT. Derangement of pulmonary extraction of 5-HT also may be related to the occurrence of postoperative venous thrombosis (8). Both hypotheses depend on the direct demonstration in man that 5-HT is removed from the pulmonary vascular space.…”

mentioning

confidence: 99%

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Pulmonary Extraction of 5-Hydroxytryptamine and Norepinephrine before and after Cardiopulmonary Bypass in Man

Gillis

Greene

Cronau

et al. 1972

Circulation Research

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Pulmonary extraction of 14 C-5-hydroxytryptamine and 3 H-norepinephrine was estimated in patients undergoing aortocoronary saphenous vein grafting. Identical mixtures of both amines were administered intravenously before cardiopulmonary bypass and again just after bypass. Immediately after each injection, 6 ml of blood was withdrawn into tubing, at a constant rate, simultaneously from both the pulmonary artery and the left atrium. Each set of tubing was then divided into six segments, and the 3 H and 14 C content of each segment was measured. In this manner, total isotope collected and blood isotope concentration as a function of time at the two sampling sites were compared directly. Before bypass in every patient studied, less 5-hydroxytryptamine and norepinephrine were withdrawn on the left than on the right of the lungs, implying pulmonary extraction of both amines. In nine patients, the mean percent extraction was 65 ± 4% for 5-hydroxytryptamine and 23 ± 5% for norepinephrine ( P < 0.005). After bypass, the percent extraction of both norepinephrine and 5-hydroxytryptamine was increased in all but one patient; values for norepinephrine were increased to a realtively greater extent. These data represent a direct demonstration of 5-hydroxytryptamine and norepinephrine extraction by human lungs and also suggest that total cardiopulmonary bypass may alter the process.KEY WORDS lung aortocoronary bypass pulmonary vascular space amine extraction• Both 5-hydroxytryptamine (5-HT) and norepinephrine (NE) are removed, to varying degrees, from the pulmonary vascular space of dog (1-4), cat (5), rat (6, 7), guinea pig (8), and rabbit (9). Pulmonary venous and, thus, systemic arterial blood concentrations of these amines are significantly decreased by passage through the lung. The mechanisms and possible physiological significance of the process are unknown, though it has been suggested (10) that pulmonary clearance prevents vasoactive substances (including both NE and 5-HT) which are present inFrom the

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Section: Amine Removal By Human Lungmentioning

confidence: 50%

mentioning

confidence: 99%

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confidence: 99%

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Pulmonary Extraction of 5-Hydroxytryptamine and Norepinephrine before and after Cardiopulmonary Bypass in Man

Gillis

Greene

Cronau

et al. 1972

Circulation Research

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“…The pulmonary circulation inactivates 90-95% of the bradykinin passing through it by enzymic attack without any evidence of a preliminary uptake step, and this process may be contrasted with the combined uptake and enzymic oxidation process that inactivates a comparably high proportion of 5-hydroxytryptamine passing through the pulmonary circulation (Alabaster & Bakhle, 1970;Gruby, Rowlands, Varley & Wyllie, 1971). The ability of the pulmonary circulation to inactivate two such dissimilar substances emphasizes the multiple metabolic capabilities of this vascular bed and its potential in determining the pharmacodynamics of such substances.…”

Section: Discussionmentioning

confidence: 99%

The inactivation of bradykinin in the pulmonary circulation of isolated lungs

Alabaster

Bakhle

1972

British J Pharmacology

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Summary1. The isolated lungs of guinea-pigs, rats and dogs, perfused with Krebs bicarbonate solution via the pulmonary artery, inactivated 95, 98 and 99% respectively of the bradykinin infused through them. 2. This inactivation process was not inhibited by 2-mercaptoethanol (1 mM) or EDTA (500 ,UM).3. The inactivation was inhibited by 2: 3-dimercaptopropanol (100 /.LM), N-ethylmaleimide (100 /,M), and several o fthe bradykinin potentiating peptides from Bothrops jararaca, in both natural and synthetic forms. 4. The effect of these compounds, 2-mercaptoethanol, EDTA, 2: 3-dimercaptopropanol, N-ethylmaleimide and Bothrops peptides on the pulmonary bradykininase activity is the same as their effect on pulmonary angiotensin I converting enzyme.

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“…Inactivation occurs by a process involving carrier-mediated uptake fol lowed by metabolism to 5-hydroxyindoleacetic acid (5-H1AA) [1][2][3]. Radioauto graphic localization has confirmed that pulmonary endothelial cells are the site of serotonin uptake [4], The lung is also cap able of storing serotonin and these storage sites have been identified in neuroendo crine cells [5].…”

Section: Introductionmentioning

confidence: 99%

Serotonin Receptors in Rat Lung

Das¹,

Steinberg²

1986

Respiration

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Mammalian lungs have been shown to store and to inactivate serotonin by an active process involving uptake and metabolism. Serotonin has direct action on lung including constrictor effects of pulmonary vascular and tracheobronchial smooth muscle suggesting the presence of serotonin receptors in lung. We have identified several serotonin binding receptors in rat lung. Two separate binding sites are present in a purified mitochondrial fraction. Saturation analysis of (³H)-serotonin binding to outer mitochondrial membranes exhibits temperature-dependent association kinetics and demonstrates a single, high affinity, high capacity binding (dissociation constant = 8.3 ± 1.2 nM, maximum binding capacity = 0.819 ± 0.046 pmol/mg protein). The dissociation constant of inner mitochondrial membrane demonstrates a low affinity, low capacity site (dissociation constant = 25.2 +2.2 nM, maximum binding capacity = 0.453 ± 0.037 pmol/mg protein). The purified microsomal fraction of lung exhibits a moderate affinity, high capacity binding site for (³H)-serotonin (dissociation constant = 14.8 ± 1.6 nM, maximum binding capacity = 0.760 ± 0.03 pmol/mg protein). In addition to the lung being the major site for its inactivation, the presence of several specific serotonin receptors may be related to some of the known serotonin actions in lung and may suggest other unknown actions of this amine.

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The fate of 5-hydroxytryptamine in the lungs

Cited by 28 publications

References 13 publications

Pulmonary Extraction of 5-Hydroxytryptamine and Norepinephrine before and after Cardiopulmonary Bypass in Man

Pulmonary Extraction of 5-Hydroxytryptamine and Norepinephrine before and after Cardiopulmonary Bypass in Man

The inactivation of bradykinin in the pulmonary circulation of isolated lungs

Serotonin Receptors in Rat Lung

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