Platelet function and anesthetics in cardiac surgery:: An in vitro and ex vivo study

被引:26
|
作者
Parolari, A
Guarnieri, D
Alamanni, F
Toscano, T
Tantalo, V
Gherli, T
Colli, S
Foieni, F
Franzè, V
Stanghellini, M
Gianotti, GA
Biglioli, P
Tremoli, E
机构
[1] Univ Milan, Dept Cardiac Surg, Ctr Cardiol, Fondazione Monzino IRCCS, I-20138 Milan, Italy
[2] Transfus Ctr, Ist Clinci Perfezionamento, Milan, Italy
[3] Univ Parma, Dept Cardiac Surg, I-43100 Parma, Italy
[4] Univ Milan, Inst Pharmacol Sci, Milan, Italy
[5] Ctr Cardiol IRCCS, Clin Pathol Lab, Milan, Italy
来源
ANESTHESIA AND ANALGESIA | 1999年 / 89卷 / 01期
关键词
D O I
10.1097/00000539-199907000-00005
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
We studied the effects of the anesthetics commonly used in cardiac surgery on platelet function. Fentanyl, droperidol, succinylcholine, pancuronium, thiopental, and diazepam at therapeutic concentrations were tested for their in vitro effects on the expression of platelet membrane glycoproteins Ib and IIbIIIa (GpIb, GpIIb-IIIa) and of P-selectin in anticoagulated whole blood by flow cytometry. The expression of P-selectin was determined under basal conditions, after the incubation of blood with adenosine diphosphate (ADP) 10 mu mol/L, and the stable prostaglandin endoperoxide analog U46619 1 mu mol/L. No drug affected the expression of P-selectin in unstimulated and ADP- or US6619-stimulated platelets, with the exception of thiopental, which markedly decreased the U46619-induced expression of P-selectin. Thiopental concentration-dependently inhibited U46619-induced and ADP-induced platelet aggregation, with effects on U46619-induced aggregation at therapeutic concentrations. To assess au vivo effects, the same platelet markers were also assessed in blood obtained from 10 patients undergoing elective coronary surgery, Compared with basal values, platelet response to U46619 was significantly reduced just after the administration of anesthetic drugs, and the effect persisted for 48 h after surgery. Our study suggests that, at therapeutic concentrations, thiopental inhibits U46619-induced platelet activation bo th in vitro and ex vivo. The mechanisms responsible of this effect, together with its clinical significance, require further investigation Implications: Thiopental inhibited prostaglandin-induced platelet activation at therapeutic concentrations both in vitro and ex vivo in cardiac surgical patients whereas adenosine diphosphate-induced activation was affected only at supratherapeutic drug concentrations. Thus, administration of sodium thiopental may contribute to the in vivo impairment of platelet function in patients undergoing elective cardiac surgery.
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收藏
页码:26 / 31
页数:6
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