Impact of obstructive sleep apnoea and intermittent hypoxia on blood rheology: a translational study.
Journal
The European respiratory journal
ISSN: 1399-3003
Titre abrégé: Eur Respir J
Pays: England
ID NLM: 8803460
Informations de publication
Date de publication:
10 2021
10 2021
Historique:
received:
04
02
2021
accepted:
08
04
2021
pubmed:
18
4
2021
medline:
28
10
2021
entrez:
17
4
2021
Statut:
epublish
Résumé
Haemorheological alterations are reported in obstructive sleep apnoea (OSA) and reversed with continuous positive airway pressure (CPAP), observations potentially explained by intermittent hypoxia (IH)-induced oxidative stress. Our objective was to investigate whether IH causes haemorheological alterations Wistar rats were exposed to normoxia (n=7) or IH (n=8) for 14 days. 23 moderate-to-severe OSA patients were assessed at three time-points: baseline, after randomisation to either 2 weeks of nocturnal oxygen (n=13) or no treatment (n=10) and after 1 month of CPAP treatment (n=17). Furthermore, an OSA-free control group (n=13) was assessed at baseline and after time-matched follow-up. We measured haemorheological parameters (haematocrit, blood viscosity, plasma viscosity (rats only), erythrocyte aggregation and deformability (humans only)) and redox balance (superoxide dismutase (SOD), glutathione peroxidase, protein oxidation (advanced oxidation protein products (AOPPs)) and lipid peroxidation (malondialdehyde)). We also tested the haemorheological sensitivity of erythrocytes to reactive oxygen species (ROS) in our human participants using the oxidant In rats, IH increased blood viscosity by increasing haematocrit without altering the haemorheological properties of erythrocytes. IH also reduced SOD activity and increased AOPPs. In humans, baseline haemorheological properties were similar between patients and control participants, and properties were unaltered following oxygen and CPAP, except erythrocyte deformability was reduced following oxygen therapy. Redox balance was comparable between patients and control participants. At baseline, TBHP induced a greater reduction of erythrocyte deformability in patients while CPAP reduced TBHP-induced increase in aggregation strength. IH and OSA
Sections du résumé
BACKGROUND
Haemorheological alterations are reported in obstructive sleep apnoea (OSA) and reversed with continuous positive airway pressure (CPAP), observations potentially explained by intermittent hypoxia (IH)-induced oxidative stress. Our objective was to investigate whether IH causes haemorheological alterations
METHODS
Wistar rats were exposed to normoxia (n=7) or IH (n=8) for 14 days. 23 moderate-to-severe OSA patients were assessed at three time-points: baseline, after randomisation to either 2 weeks of nocturnal oxygen (n=13) or no treatment (n=10) and after 1 month of CPAP treatment (n=17). Furthermore, an OSA-free control group (n=13) was assessed at baseline and after time-matched follow-up. We measured haemorheological parameters (haematocrit, blood viscosity, plasma viscosity (rats only), erythrocyte aggregation and deformability (humans only)) and redox balance (superoxide dismutase (SOD), glutathione peroxidase, protein oxidation (advanced oxidation protein products (AOPPs)) and lipid peroxidation (malondialdehyde)). We also tested the haemorheological sensitivity of erythrocytes to reactive oxygen species (ROS) in our human participants using the oxidant
RESULTS
In rats, IH increased blood viscosity by increasing haematocrit without altering the haemorheological properties of erythrocytes. IH also reduced SOD activity and increased AOPPs. In humans, baseline haemorheological properties were similar between patients and control participants, and properties were unaltered following oxygen and CPAP, except erythrocyte deformability was reduced following oxygen therapy. Redox balance was comparable between patients and control participants. At baseline, TBHP induced a greater reduction of erythrocyte deformability in patients while CPAP reduced TBHP-induced increase in aggregation strength.
CONCLUSIONS
IH and OSA
Identifiants
pubmed: 33863746
pii: 13993003.00352-2021
doi: 10.1183/13993003.00352-2021
pii:
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : CIHR
Pays : Canada
Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright ©The authors 2021. For reproduction rights and permissions contact permissions@ersnet.org.
Déclaration de conflit d'intérêts
Conflict of interest: X. Waltz has nothing to disclose. Conflict of interest: A.E. Beaudin reports other (scholarships) from the Canadian Institutes of Health Research – Heart and Stroke Foundation of Canada (HSFC), Alberta Innovates – Health Solutions (AIHS), and University of Calgary, during the conduct of the study. Conflict of interest: E. Belaidi has nothing to disclose. Conflict of interest: J. Raneri has nothing to disclose. Conflict of interest: J-L. Pépin reports grants and other (research funds) from Air Liquide Foundation, grants, personal fees and other (research funds) from Agiradom, AstraZeneca, Philips and ResMed, grants and personal fees from Fisher and Paykel, Mutualia and Vitalaire, personal fees from Boehringer Ingelheim, Jazz Pharmaceutical, Night Balance and Sefam, outside the submitted work. Conflict of interest: V. Pialoux has nothing to disclose. Conflict of interest: P.J. Hanly has nothing to disclose. Conflict of interest: S. Verges has nothing to disclose. Conflict of interest: M.J. Poulin has nothing to disclose.