TY - GEN
T1 - NC1900, an arginine vasopressin analogue, fails to reduce brain edema and improve neurobehavioral deficits in an intracerebral hemorrhagic stroke mice model
AU - Manaenko, Anatol
AU - Lekic, Tim
AU - Zhang, John H.
AU - Tang, Jiping
N1 - Funding Information:
Acknowledgement This study is partially supported by NIH NS053407 to J.H. Zhang and NS060936 to J. Tang. Conflict of interest statement
PY - 2011
Y1 - 2011
N2 - 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. Materials and 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.
AB - 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. Materials and 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.
KW - Arginine vasopressin
KW - Brain edema
KW - ICH
KW - Neuroprotection
UR - http://www.scopus.com/inward/record.url?scp=79960683127&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=79960683127&partnerID=8YFLogxK
U2 - 10.1007/978-3-7091-0693-8_26
DO - 10.1007/978-3-7091-0693-8_26
M3 - Conference contribution
C2 - 21725748
SN - 9783709106921
T3 - Acta Neurochirurgica, Supplementum
SP - 155
EP - 159
BT - Intracerebral Hemorrhage Research
PB - Springer-Verlag Wien
ER -