PLATELET FACTOR-4 RELEASE IN PATIENTS UNDERGOING CARDIOPULMONARY-RESUSCITATION - CAN REPERFUSION BE IMPAIRED BY PLATELET ACTIVATION

Citation
Bw. Bottiger et al., PLATELET FACTOR-4 RELEASE IN PATIENTS UNDERGOING CARDIOPULMONARY-RESUSCITATION - CAN REPERFUSION BE IMPAIRED BY PLATELET ACTIVATION, Acta anaesthesiologica Scandinavica, 40(5), 1996, pp. 631-635
Citations number
31
Categorie Soggetti
Anesthesiology
ISSN journal
00015172
Volume
40
Issue
5
Year of publication
1996
Pages
631 - 635
Database
ISI
SICI code
0001-5172(1996)40:5<631:PFRIPU>2.0.ZU;2-2
Abstract
Background: Reperfusion following cardiac arrest is associated with a marked activation of blood coagulation. This seems to be associated wi th microcirculatory reperfusion disorders. The present study was desig ned to investigate the possible involvement of platelets in reperfusio n injury following cardiac arrest. Plasma levels of platelet factor 4 (PF 4) were used as an indicator for in vivo platelet activation becau se PF 4 is known to be released from platelets during aggregation. Met hods: Plasma PF 4 levels (normal range: < 5 IU/mL) were measured in 18 patients at predetermined time points during cardiopulmonary resuscit ation (CPR). In the case of restoration of spontaneous circulation, ad ditional blood samples were analyzed until seven days after stabilizat ion. The PF 4 levels of four sex-matched volunteers were used as contr ols. Results: The median of the maximum individual PF 4 levels measure d during CPR was 27.5 IU/mL (range 1.2 to 90 IU/mL; P < 0.01 versus co ntrols). Compared with PF 4 levels in control volunteers (median: 0.35 IU/mL; range 0.2 to 0.6 IU/mL) PF 4 levels were significantly elevate d in patients during CPR and in the early phase until 24 hours after r estoration of spontaneous circulation (P < 0.05). Conclusion: A marked increase in PF 4 levels was observed during CPR and in the early phas e after cardiac arrest in man. This increase in PF 4 levels has to be viewed as an indicator of platelet activation, which may play a role i n the etiology of reperfusion injury and microcirculatory reperfusion disorders occurring after cardiac arrest.