Background
Medetomidine (MED) is used for animal experiment as mixed anesthesia (Medetomidine-Midazolam-Butorphanol: MMB). On the other hand, Dexmedetomidine (DEX), its enantiomer, is used for human sedation in the intensive care situation. It is unknown whether or not they may accelerate thrombogenesis via platelets α2-receptors stimulation and we evaluate their effect on platelet aggregation and thrombotic vessel occlusion using animal model.
Method
ICR mice (6-month-old males) were used for the experiments.
1) Blood was collected under pentobarbital anesthesia (80 mg/kg-i.p.), and collagen (0.8 µg/mL)-induced platelet aggregation was measured under DEX or MED supplementation.
2) Mice were injected with 1 µg/kg DEX or 0.75 mg/kg MED i.p., before pentobarbital 80mg/kg anesthesia, and p­latelet aggregation was evaluated similarly as described above.
3) Vascular occlusion time was measured by ferric chloride (FeCl3)-induced thrombosis models under MMB or pentobarbital anesthesia.
Results
1) Platelet aggregation was enhanced by higher concentrations at 10 ng/mL DEX or 100 ng/mL MED supplement. The lower concentrations under 1 ng/mL DEX or 10 ng/mL MED did not affect aggregation.
2) 1 µg/kg MED i.p. enhanced platelet aggregation, while 0.75 mg/kg DEX did not.
3) Thrombotic occlusion time of mice femoral artery was shortened in MMB-anesthetized animals in comparison with pentobarbital-anesthetized ones.
Discussion
Clinical doses of DEX seem not affect thrombogenicity, while MED in MMB-animal anesthesia was revealed to enhance it.