PLATELET ACTIVATION WITH MASSIVE FORMATION OF THROMBOXANE A(2) DURINGAND AFTER CARDIOPULMONARY-RESUSCITATION

Objective: Hypoxia and ischemia cause endothelial cell damage with con sequent platelet activation. The hypothesis that human cardiac arrest accelerates platelet activation and the formation of prostanoids was t ested. Design: Prospective, observational cohort study. Setting: Emerg ency Department and general Intensive Care Unit in a city hospital. In terventions: Basic and advanced life support. Patients and participant s: Forty-seven out-of-hospital cardiac arrest patients. The patients w ere classified into two groups, those who were resuscitated (n=18) and those who died (n=29). Measurements and results: Serial levels of pla telet aggregation, thromboxane B-2 (TXB(2)), 11-dehydro-TXB(2) and 6-k eto-prostaglandin F-1 alpha (6-keto-PGF(1) alpha) were measured. The r esults of measurements and demographic data were compared between the groups. Platelet counts decreased at the end of cardiopulmonary resusc itation (CPR), the decrease of the platelet counts showed statistical significance especially in the patients who died (p<0.001). Platelet a ggregation induced by adenosine diphosphate, epinephrine and collagen decreased to the lower limits of normal during and after CPR. Although high values of TXB(2) and 11-dehydro-TXB(2) continued throughout the study period in the resuscitated patients, 6-keto-PGF(1) alpha decreas ed to the normal range (22.7 +/- 3.6 pg . ml(-1), p<0.05) at 24 h afte r arrival at the Emergency Department. Conclusions: Platelet activatio n with the massive formation of thromboxane A(2) (TXA(2)) occurs in pa tients with out-of-hospital cardiac arrest. Successful resuscitation i s not associated with the balanced production of PGI(2) against the TX A(2) formation.