Abstract
Objective
To evaluate the effects of hyperbaric oxygen (HBO) therapy on the coagulation cascade using an experimental model of multiple organ failure syndrome (MOFS).
Design
MOFS was induced by zymosan (500 mg/kg i. p.) in rats. HBO therapy (2 ATA) was administered in a cylindrical steel chamber 4 and 11 h after zymosan administration. In a separate set of experiments animals were monitored for 72 h, and systemic toxicity was scored.
Intervention
Eighteen hours after zymosan administration, rats were killed and blood samples were used for analysis of hemocoagulative parameters, hemodynamics, and arterial blood gas.
Main results
Zymosan administration caused MOFS by affecting the coagulation cascade, as shown by a significant increase in plasma levels of fibrinogen, tissue plasminogen activator, inhibitor of tissue plasminogen activator of type 1, and plasma levels of fibrin degradation products vs. control rats. Zymosan-induced MOFS was also characterized by a significant increase in von Willebrand antigen plasma levels vs. controls. Moreover, zymosan administration induced a significant fall in mean arterial blood pressure and alteration in blood gas values. HBO therapy significantly reduced the derangements of coagulation cascade, the fall in mean blood pressure and alteration in blood gas induced by zymosan administration.
Conclusions
The hypercoagulability induced by zymosan could be responsible for organ failure and death. Our data demonstrate that HBO therapy significantly prevents the alteration in the coagulation cascade and arterial blood gas in an experimental model of MOFS.
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Acknowledgements
This study was supported by a grant from the Undersea and Hyperbaric Medicine Society. We are grateful to Jean Gilder for editing the text.
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This article is discussed in the editorial available at:http://dx.doi.org/10.1007/s00134-006-0379-z.
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Imperatore, F., Cuzzocrea, S., De Lucia, D. et al. Hyperbaric oxygen therapy prevents coagulation disorders in an experimental model of multiple organ failure syndrome. Intensive Care Med 32, 1881–1888 (2006). https://doi.org/10.1007/s00134-006-0367-3
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DOI: https://doi.org/10.1007/s00134-006-0367-3