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Abrupt oxygen decrease influences thrombosis and bleeding in stenosed and endothelium-injured rabbit carotid arteries

Published online by Cambridge University Press:  01 December 2008

J. Dellamonica,
E. Mazoyer,
J. P. Rosa,
F. Cymbalista and
ChM. Samama
J. Dellamonica
Affiliation:
Avicenne University Hospital, Department of Anaesthesiology and Intensive Care, Bobigny, Paris, France
E. Mazoyer
Affiliation:
Avicenne University Hospital, Laboratory of Haematology, Bobigny, Paris, France
J. P. Rosa
Affiliation:
Avicenne University Hospital, Lariboisière Hospital, INSERM U689, Paris, France
F. Cymbalista
Affiliation:
Avicenne University Hospital, Laboratory of Haematology, Bobigny, Paris, France
ChM. Samama*
Affiliation:
Avicenne University Hospital, Department of Anaesthesiology and Intensive Care, Bobigny, Paris, FranceAvicenne University Hospital, Lariboisière Hospital, INSERM U689, Paris, France
*
Correspondence to: Charles Marc Samama, Department of Anaesthesiology and Intensive Care, Hotel-Dieu University Hospital 1, place du Parvis de Notre-Dame, 75181 Paris Cedex 04, France. E-mail: marc.samama@htd.aphp.fr; Tel: +33 1 42 34 85 51; Fax: +33 1 42 34 89 60
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Summary

Background and objective

Blood oxygen concentration decrease may be associated with haemostatic impairments. We aimed to study the effect of oxygen decrease in a rabbit model of thrombosis and bleeding.

Methods

A total of 44 rabbits were anaesthetized, ventilated and monitored for blood pressure, blood arterial gas, temperature and carotid blood flow. The Folts model was used: a stenosis (75%) and an injury were carried out on the carotid artery, inducing thrombosis. Blood flow decreased as thrombus size increased until the pressure gradient was such that the thrombus was released and local arterial blood flow was suddenly restored. This is known as a cyclic flow reduction. After counting baseline cyclic flow reductions during a 20-min period (P1), rabbits were randomized blindly to one of three groups: hyperoxic, FiO2=100%; normoxic, FiO2 was decreased to obtain a PaO2 between 80 and 120 mmHg; hypoxic, PaO2 < 80 mmHg. Then CFRs were recorded over a second 20-min period (P2). At the end of the experiment, a hepatosplenic section was done and the amount of blood loss was recorded. After each period, the following parameters were measured: blood gas, ear-immersion bleeding time, haemoglobin, platelet count, prothrombin time, activated partial thromboplastin time and fibrinogen.

Results

Oxygen decrease during hypoxic and normoxic periods was associated with a decrease in cyclic flow reductions. Bleeding time increased in the hypoxic group unless hepatosplenic bleeding remained stable. A slight increase in activated partial thromboplastin time was observed in the normoxic and hypoxic groups.

Conclusion

An abrupt decrease in oxygen administration was responsible for an antithrombotic effect. Increase in bleeding time occurred during hypoxia. No clinically relevant variation of any haemostasis parameters was observed.

Keywords

CAROTID ARTERY THROMBOSISHAEMORRHAGEPLATELET AGGREGATIONOXYGENATIONHYPOXIARABBIT

Information

Type
Original Article
Information
European Journal of Anaesthesiology , Volume 25 , Issue 12 , December 2008, pp. 1002 - 1008
Copyright
Copyright © European Society of Anaesthesiology 2008

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