Experimental Physiology
	

Celebrating 100 years
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


Physiology in Press

First published online on February 22, 2005.
Experimental Physiology (2005)
DOI: 10.1113/expphysiol.2004.029306
© The Physiological Society 2005

A more recent version of this article appeared on May 1, 2005
This Article
Right arrow Full Text (Rapid PDF)
Right arrow All Versions of this Article:
90/3/411    most recent
expphysiol.2004.029306v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Dunleavy, M.
Right arrow Articles by Bradford, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dunleavy, M.
Right arrow Articles by Bradford, A.

Received October 11, 2004
Revised December 23, 2004
Accepted after revision February 10, 2005


Respiratory physiology

Chronic intermittent asphyxia increases platelet reactivity in rats

Mark Dunleavy 1, Michelle Dooley 1, Dermot Cox 1, Aidan Bradford 1*

1 Royal College of Surgeons in Ireland

* To whom correspondence should be addressed. E-mail: abradfor{at}rcsi.ie.


   Abstract
Sleep disordered breathing is associated with chronic intermittent asphyxia and with a variety of cardiovascular abnormalities. Cardiovascular morbidity and mortality are linked to altered platelet function and platelet function is affected in sleep disordered breathing. Since there is evidence that chronic continuous hypoxia may alter platelet number and function, the present study tests the hypothesis that chronic intermittent asphyxia affects platelet count, activation and aggregation. Rats were treated with a hypercapnic hypoxic gas mixture (minimum of 6-8% O2, maximum of 10-14% CO2) for 15 seconds, twice per minute for 8 hours per day for 3 weeks. Blood was analysed for platelet count, platelet activation (CD62p expression using flow cytometry), response to low dose ADP, haematocrit, red cell count and haemoglobin concentration. A Platelet Function Analyser measured the closure time of an aperture, dependent on platelet aggregation. Compared to controls (n=16), chronic intermittent asphyxia (n=13) reduced body weight and increased right ventricular weight but had no significant effect on platelet count (control: 880.4±20.1; treated: 914.1±35.2 X103/µl; mean±SE), on the reduction in platelet count in response to ADP (reduced to 206.7±49.0 and 193.8±35.9 X103/µl for control and treated respectively), or on the percentage of platelets positive for CD62p (control: 5.2±0.7; treated: 6.0±0.8%). Chronic intermittent asphyxia significantly (p=0.037) reduced the closure time (control: 90.9±7.7; treated: 77.7±3.8 seconds), indicating greater adhesion and aggregation. There was no significant difference in haematocrit, red cell count and haemoglobin concentration. In conclusion, chronic intermittent asphyxia has no effect on platelet count but does increase platelet aggegation in rats. These data support the idea that chronic intermittent asphyxia alters platelet function in sleep disordered breathing.

Key Words: Apnoea, Hypoxia, Platelet







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Copyright © 2005 by the The Physiological Society.