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Acute hyperoxaemia-induced effects on regional blood flow, oxygen consumption and central circulation in man
Linköping University, Department of Medical and Health Sciences, Anesthesiology. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Medical and Health Sciences, Anesthesiology. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Medicine and Care, Clinical Physiology. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Medical and Health Sciences, Anesthesiology. Linköping University, Faculty of Health Sciences.
2005 (English)In: Acta Physiologica Scandinavica, ISSN 0001-6772, E-ISSN 1365-201X, Vol. 183, no 3, 231-240 p.Article in journal (Refereed) Published
Abstract [en]

Aim:  Despite numerous in vitro and animal studies, circulatory effects and mechanisms responsible for the vasoconstriction seen during hyperoxaemia are yet to be ascertained. The present study set out to: (i) set up a non-invasive human model for the study of hyperoxia-induced cardiovascular effects, (ii) describe the dynamics of this effect and (iii) determine whether hyperoxaemia also, by vasoconstriction alters oxygen consumption (O2).

Methods:  The study comprised four experiments (A, B, C and D) on healthy volunteers examined before, during and after 100% oxygen breathing. A: Blood flow (mL min−1·100 mL−1 tissue), venous occlusion plethysmography was assessed (n = 12). B: Blood flow was recorded with increasing transcutaneous oxygen tension (PtcO2) levels (dose–response) (n = 8). C: Heart rate (HR), stroke volume, cardiac output (CO) and systemic vascular resistance (SVR) was assessed using echocardiography (n = 8). D: O2 was measured using an open circuit technique when breathing an air-O2 mix (fraction of inhaled oxygen: FiO2 = 0.58) (n = 8).

Results:  Calf blood flow decreased 30% during O2 breathing. The decrease in calf blood flow was found to be oxygen dose dependent. A similar magnitude, as for the peripheral circulation, of the effect on central parameters (HR/CO and SVR) and in the time relationship was noted. Hyperoxia did not change O2. An average of 207 (93) mL O2 per subject was washed in during the experiments.

Conclusion:  This model appears suitable for the investigation of O2-related effects on the central and peripheral circulation in man. Our findings, based on a more comprehensive (central/peripheral circulation examination) evaluation than earlier made, suggest significant circulatory effects of hyperoxia. Further studies are warranted to elucidate the underlying mechanisms.

Place, publisher, year, edition, pages
2005. Vol. 183, no 3, 231-240 p.
Keyword [en]
blood flow, consumption, hyperoxaemia, hyperoxia, oxygen, vasoconstriction
National Category
Medical and Health Sciences
URN: urn:nbn:se:liu:diva-24768DOI: 10.1111/j.1365-201X.2005.01405.xLocal ID: 7029OAI: diva2:245091
Available from: 2009-10-07 Created: 2009-10-07 Last updated: 2012-10-02Bibliographically 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.
Linköping University Medical Dissertations, ISSN 0345-0082 ; 891
National Category
Medical and Health Sciences
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)
Available from: 2009-10-09 Created: 2009-10-09 Last updated: 2012-10-03Bibliographically approved

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