The Journal of Trauma: Injury, Infection, and Critical Care · 2004 · 91 citations · 33 references
MedicineNeurosciencePharmacologyBehavioral NeuroscienceNeuropharmacologyPharmacodynamicsCellular InjuryNeuroprotectionNeuroprotective PharmacologyAcoustic Startle ResponseBlast-related Traumatic Brain InjuryNeurobehavioral AlterationsNeurobiological Effects Of TraumaNeuroprotective AgentsNeuroprotective MechanismsReduced Grip StrengthRodent Brain Injury
BACKGROUND: The present study investigated the neuroprotective role of aminoguanidine, a known inducible nitric oxide synthase inhibitor, in both behavioral and morphologic changes in rats subjected to nonpenetrative blast injury. METHODS: Male Sprague-Dawley rats were randomly divided into groups to receive either normal saline or aminoguanidine (AG) before or after exposure to two blast dosages of either 2.8 or 20 kPa. The neurobehavioral alterations were determined by subjecting the animals to rotametric, grip-strength, passive avoidance, total and ambulatory locomotor activities, and acoustic startle response tests. RESULTS: Exposure to blast at 20 kPa resulted in a significant performance decrement on rotametric and grip-strength tests in rats treated with normal saline. In contrast, animals receiving AG either prophylactically before or after the blast seemed unaffected by the same blast. This finding also correlates well with histologic examination that showed a reduction in degenerating cortical neurons in AG-treated rats compared with those receiving saline injection. CONCLUSION: It is thus suggested that AG could play a neuroprotective role in rats subjected to blast exposure.
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