NC1900, an arginine vasopressin analogue, fails to reduce brain edema and improve neurobehavioral deficits in an intracerebral hemorrhagic stroke mice model.
Mots clés
Abstrait
OBJECTIVE
There is mounting evidence suggesting that arginine vasopressin via its V1a receptor interaction is involved in the regulation of the brain water channel, aquaporin-4 (AQP4). The role of AQP4 in brain edema resolution has been thoroughly investigated in knock-out animal studies, which showed that its depletion increases brain water content in models of vasogenic edema. As a result, we tested the hypothesis that the activation of V1a receptor by it selective agonist will decrease brain edema in a mouse intracerebral hemorrhage (ICH) model.
METHODS
ICH was induced by injection of bacterial collagenase into the right basal ganglia in CD1 male mice (weight 30-35 g). The animals were divided into the following groups: sham, ICH+vehicle, and ICH+AVP V1a receptor agonist. Brain edema and neurological outcomes were evaluated at 24 and 72 h post-ICH.
RESULTS
We found that collagenase injection increased brain edema and resulted in subsequent neurobehavioral deficits at both time points. Treatment with our agonist had no effect on the ICH outcomes at both time points.
CONCLUSIONS
Our results suggest that the activation of the V1a receptor has no beneficial effect on secondary brain injury following ICH in mice.
