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Hyperoxaemia does not change concentrations of serotonin and beta‐thromboglobulin in blood of healthy humans
Linköping University, Department of Medical and Health Sciences, Anesthesiology. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Biomedicine and Surgery, Plastic Surgery, Hand Surgery and Burns. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Biomedicine and Surgery, Plastic Surgery, Hand Surgery and Burns. Linköping University, Faculty of Health Sciences.
2004 (English)In: Scandinavian Journal of Clinical and Laboratory Investigation, ISSN 0036-5513, E-ISSN 1502-7686, Vol. 64, no 2, 81-85 p.Article in journal (Refereed) Published
Abstract [en]

Background: The mechanisms of oxygen‐induced effects on blood vessels (vasoconstriction in hyperoxaemia and vasodilatation during hypoxaemia) are uncertain. Many investigators have suggested that the vasoconstriction seen during hyperoxia/hyperoxaemia is mediated through the endothelium as a result of either increased release or activity of vasoconstrictors (oxygen radicals, endothelin, norepinephrine, angiotensin II, or serotonin (5‐HT)), or reduced activity of vasodilators (prostaglandin E2 and nitric oxide). Serotonin has been assumed to have a central role.

Methods: Eight healthy volunteers were exposed to FiO2 of 1.0 for 20 min and serum concentrations of serotonin and activated platelets were measured (indicated by concentrations of β‐thromboglobulin (β‐TG)).

Results. During hyperoxaemia in humans, serum concentrations of serotonin and β‐TG remained unchanged.

Conclusion: If serotonin is involved in oxygen‐induced vasoconstriction, the mechanism is more likely to be either a potentiating effect of serotonin on other vasoconstrictors or increased activity of serotonin on its receptor.

Place, publisher, year, edition, pages
2004. Vol. 64, no 2, 81-85 p.
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-24029DOI: 10.1080/00365510410004137Local ID: 3584OAI: oai:DiVA.org:liu-24029DiVA: diva2:244345
Available from: 2009-10-07 Created: 2009-10-07 Last updated: 2017-12-13Bibliographically approved
In thesis
1. Vascular effects of hyperoxaemia and its mechanisms in man
Open this publication in new window or tab >>Vascular effects of hyperoxaemia and its mechanisms in man
2005 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Most cells in the human body cannot survive without oxygen. The regulation of oxygen delivery to meet demands of tissues remains contentious. The study of supranormallevels of oxygen (hyperoxia/hyperoxaemia) may contribute to the understanding, as mechanisms that are active during normoxia and hypoxia (oxygen deficit) can be assumed to be at least similar, and compensatory mechanisms are kept to a minimum. Hyperoxaemic conditions are often seen clinically, but their effects in the human body are not fully known.

Hyperoxaemia causes vasoconstriction and reduction in heart rate and cardiac output. These effects are thought to be mediated through the endothelium as a result of either increased release, or activity, of vasoconstrictors such as serotonin (5-hydroxytryptamine, 5-HT)), or reduced activity of vasodilators such as prostaglandin E2 and nitric oxide (NO)). 5-HT and NO have been thought to have a central role.

To investigate both its effects and the underlying mechanisms we set up a human non-invasive normobaric hyperoxaemic model. We studied the effects of hyperoxaemia by measuring: peripheral blood flow by venous occlusion plethysmography; skin blood flow by laser Doppler perfusion imaging (LDI); cardiovascular assessments by echocardiography; and oxygen consumption (VO2) by an open circuit exchange system, CPX.

Plasma concentrations of 5-HT and ß-thromboglobulin (ß-TG) were measured to investigate the role of 5-HT during hyperoxaemia. To test the NO-hypothesis we achieved endothelium-dependent and endothelium-independent vasodilatation, using acetylcholine (ACh), and sodium nitroprusside (SNP) iontophoresis, respectively.

Mean calf blood flow decreased linearly to as much as -20% during oxygen breathing. Heart rate and cardiac output decreased, systemic vascular resistance increased, and blood pressure remained unchanged. Hyperoxaemia lessened vasodilatation in the skin induced by current (iontophoresis) and an anaesthetic agent (EMLA®-cream). There was no significant increase in concentrations of either 5-HT or ß-TG during hyperoxia, compared with air. Endothelium-dependent vasodilatation (ACh) was significantly reduced by breathing 100% oxygen. Vitamin C taken orally abolished the effects of oxygen. Hyperoxia did not affect endothelium-independent vasodilatation (SNP).

Hyperoxia affected most parts of the cardiovascular system in man, including perfusion in the skin. Probably the first and most pronounced effect was peripheral vasoconstriction, which could be seen within minutes. Heart rate and cardiac output decreased, possibly secondary to the vasoconstriction, so as to keep the blood pressure constant. There was no evidence that 5-HT had an important role in hyperoxia-mediated responses. On the contrary, the most likely hypothesis is that hyperoxic vasoconstriction is mediated by inhibition of synthesis of NO by free oxygen radicals inside the endothelial cells.

Place, publisher, year, edition, pages
Linköping: Larsson Offsettryck, 2005. 49 p.
Series
Linköping University Medical Dissertations, ISSN 0345-0082 ; 891
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-31534 (URN)17333 (Local ID)91-85299-00-6 (ISBN)17333 (Archive number)17333 (OAI)
Public defence
2005-04-22, Berzeliussalen, Hälsouniversitetets bibliotek, Linköping, 13:00 (Swedish)
Opponent
Available from: 2009-10-09 Created: 2009-10-09 Last updated: 2012-10-03Bibliographically approved

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Rousseau, AndreasAbdiu, AvniSjöberg, Folke

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