BACKGROUND AND OBJECTIVES:Dexmedetomidine is a highly selective alpha2-adrenoceptor agonist used in anesthesia for its hypnoanalgesic and cardiovascular effects. Stimulation of alpha2-adrenoceptors may determine pro and anti-platelet aggregation effects through direct and indirect mechanisms. This study aimed at determining the effects of dexmedetomidine on coagulation evaluated by thromboelastography. METHODS:Twenty four patients were randomly distributed in 3 groups: Group 1 patients received saline solution (control group), Group 2 patients received 1 microg.kg-1 dexmedetomidine in 10 minutes, followed by 0.4 microg.kg-1.h-1 infusion for 20 minutes and Group 3 patients received 0.05 mg.kg-1 midazolam. Sedated patients maintained scores 3 or 4 in Ramsays sedation scale. Blood samples were collected before and 30 minutes after the treatment for thromboelastography. RESULTS:Dexmedetomidine has significantly increased reaction time (parameter R) and decreased coagulation index in final curves as compared to initial ones. Values, however, have remained within ranges accepted as normal. This phenomenon was not observed in remaining groups. CONCLUSIONS:Dexmedetomidine pro and anti-platelet aggregation mechanisms interaction determines mild hypocoagulation, however maintaining coagulation within normal ranges. Dexmedetomidine effects on coagulation are probably not mediated by anxiolysis, since sedation was equivalent to the midazolam group.
RCT Entities:
BACKGROUND AND OBJECTIVES:Dexmedetomidine is a highly selective alpha2-adrenoceptor agonist used in anesthesia for its hypnoanalgesic and cardiovascular effects. Stimulation of alpha2-adrenoceptors may determine pro and anti-platelet aggregation effects through direct and indirect mechanisms. This study aimed at determining the effects of dexmedetomidine on coagulation evaluated by thromboelastography. METHODS: Twenty four patients were randomly distributed in 3 groups: Group 1 patients received saline solution (control group), Group 2 patients received 1 microg.kg-1 dexmedetomidine in 10 minutes, followed by 0.4 microg.kg-1.h-1 infusion for 20 minutes and Group 3 patients received 0.05 mg.kg-1 midazolam. Sedated patients maintained scores 3 or 4 in Ramsays sedation scale. Blood samples were collected before and 30 minutes after the treatment for thromboelastography. RESULTS:Dexmedetomidine has significantly increased reaction time (parameter R) and decreased coagulation index in final curves as compared to initial ones. Values, however, have remained within ranges accepted as normal. This phenomenon was not observed in remaining groups. CONCLUSIONS:Dexmedetomidine pro and anti-platelet aggregation mechanisms interaction determines mild hypocoagulation, however maintaining coagulation within normal ranges. Dexmedetomidine effects on coagulation are probably not mediated by anxiolysis, since sedation was equivalent to the midazolam group.