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Platelet activation with massive formation of thromboxane A^sub 2^ during and after cardiopulmonary resuscitation
Objective: Hypoxia and ischemia cause endothelial cell damage with consequent platelet activation. The hypothesis that human cardiac arrest accelerates platelet activation and the formation of prostanoids was tested. Design: Prospective, observational cohort study. Setting: Emergency Department and...
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Published in: | Intensive care medicine 1997-01, Vol.23 (1), p.71 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
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Summary: | Objective: Hypoxia and ischemia cause endothelial cell damage with consequent platelet activation. The hypothesis that human cardiac arrest accelerates platelet activation and the formation of prostanoids was tested. Design: Prospective, observational cohort study. Setting: Emergency Department and general Intensive Care Unit in a city hospital. Interventions: Basic and advanced life support. Patients and participants: Forty-seven out-of-hospital cardiac arrest patients. The patients were classified into two groups, those who were resuscitated (n=18) and those who died (n=29). Measurements and results: Serial levels of platelet aggregation, thromboxane B^sub 2^ (TXB^sub 2^), 11-dehydro-TXB^sub 2^ and 6-keto-prostaglandin F^sub 1^ alpha (6-keto-PGF^sub 1^ alpha) were measured. The results of measurements and demographic data were compared between the groups. Platelet counts decreased at the end of cardiopulmonary resuscitation (CPR), the decrease of the platelet counts showed statistical significance especially in the patients who died (p |
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ISSN: | 0342-4642 1432-1238 |
DOI: | 10.1007/s001340050293 |