Enhancement of platelet aggregation by tranylcypromine in mouse cerebral microvessels.
Key result
Tranylcypromine (≥10 mg/kg) enhanced platelet aggregation in mouse cerebral arterioles, providing in vivo support that prostacyclin is an inhibitor of platelet aggregation.
Why the study?
Does tranylcypromine enhance platelet aggregation in mouse cerebral microvessels?
Population
Mice (cerebral microvessels model)
Comparison
Tranylcypromine given intraperitoneally at doses… vs Iproniazid or imidazole
Design
Preclinical
Authors
Discussion
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Member takes
Implication
Does not inform clinical use; extends in vivo evidence for prostacyclin inhibiting platelet aggregation in mice.
Structured PICO
Does tranylcypromine enhance platelet aggregation in mouse cerebral microvessels?
P
Population
Mice used to study platelet aggregation in cerebral microvessels.
I
Intervention
Tranylcypromine given intraperitoneally at doses ≥ 10 mg/kg
C
Comparator
Iproniazid or imidazole
O
Outcome
Platelet aggregation in the arterioles on the cerebral surfacesurrogate
Tranylcypromine enhances platelet aggregation in vivo, supporting the hypothesis that prostacyclin acts as an endogenous inhibitor of platelet aggregation.
Cite This Study
Rosenblum et al. (1978) studied Platelet aggregation. Tranylcypromine vs. Iproniazid and Imidazole was evaluated on Platelet aggregation in the arterioles on the cerebral surface. Tranylcypromine (≥10 mg/kg) enhanced platelet aggregation in mouse cerebral arterioles, providing in vivo support that prostacyclin is an inhibitor of platelet aggregation.