There is emerging evidence to suggest that brain natriuretic peptide (BNP) is 
elevated after acute brain injury, and that it may play an adaptive role in 
recovery through augmentation of cerebral blood flow (CBF). Through a series of 
experiments, we tested the hypothesis that the administration of BNP after 
different acute mechanisms of central nervous system (CNS) injury could improve 
functional recovery by improving CBF. C57 wild-type mice were exposed to either 
pneumatic-induced closed traumatic brain injury (TBI) or collagenase-induced 
intracerebral hemorrhage (ICH). After injury, either nesiritide (hBNP) (8 
microg/kg) or normal saline were administered via tail vein injection at 30 min 
and 4 h. The mice then underwent functional neurological testing via rotorod 
latency over the following 5 days and neurocognitive testing via Morris water 
maze testing on days 24-28. Cerebral blood flow (CBF) was assessed by laser 
Doppler from 25 to 90 min after injury. After ICH, mRNA polymerase chain 
reaction (PCR) and histochemical staining were performed during the acute injury 
phase (<24 h) to determine the effects on inflammation. Following TBI and ICH, 
administration of hBNP was associated with improved functional performance as 
assessed by rotorod and Morris water maze latencies (p < 0.01). CBF was 
increased (p < 0.05), and inflammatory markers (TNF-alpha and IL-6; p < 0.05), 
activated microglial (F4/80; p < 0.05), and neuronal degeneration (Fluoro-Jade 
B; p < 0.05) were reduced in mice receiving hBNP. hBNP improves neurological 
function in murine models of TBI and ICH, and was associated with enhanced CBF 
and downregulation of neuroinflammatory responses. hBNP may represent a novel 
therapeutic strategy after acute CNS injury.