Does inhibition of angiotensin function cause neuroprotection in diffuse traumatic brain injury?

Objective(s): Neuroprotection is created following the inhibition of angiotensin II type ۱ receptor (AT۱R). Therefore, the purpose of this research was examining AT۱R blockage by candesartan in diffuse traumatic brain injury (TBI). Materials and Methods: Male rats were assigned into sham, TBI, vehicle, and candesartan groups. Candesartan (۰.۳ mg/kg) or vehicle was administered IP, ۳۰ min post-TBI. Brain water and Evans blue contents were determined, ۲۴ and ۵ hr after TBI, respectively. Intracranial pressure (ICP) and neurologic outcome were evaluated at -۱, ۱, ۴ and ۲۴ hr after TBI. Oxidant index [malondialdehyde (MDA)] was determined ۲۴ hr after TBI.Results: Brain water and Evans blue contents, and MDA and ICP levels increased in TBI and vehicle groups in comparison with the sham group. Candesartan attenuated the TBI-induced brain water and Evans blue contents, and ICP and MDA enhancement. The neurologic score enhanced following candesartan administration, ۲۴ hr after TBI.Conclusion: The blockage of AT۱R may be neuroprotective by decreasing ICP associated with the reduction of lipid peroxidation, brain edema, and blood-brain barrier (BBB) permeability, which led to the improvement of neurologic outcome.

Keywords:

Angiotensin II receptor , Blood-brain barrier , Brain edema , Brain injury , Candesartan , Intracranial pressure , Lipid Peroxidation