Korean J Anat.  2008 Mar;41(1):73-79.

Different Expressions of eNOS and AQP4 after Focal Cerebral Ischemia in Rat: In Vasogenic Edema

• Park E
• Jung Y

Abstract

Brain edema, the infiltration and accumulation of excess fluid causing an increase in brain tissue volume, often leads to a rise in intracranial pressure (ICP) and is a key contributor to the morbidity and mortality associated with brain injury. We examined the mechanisms for vasogenic brain edema produced by focal cerebral ischemia. To test the mechanisms underlying vasogenic brain edema, we compared the expression of endothelial nitric oxide synthase (eNOS) and aquaporin-4 (AQP4) in the penumbra of brain tissues after focal cerebral ischemia. The expression of eNOS and AQP4 in the ischemic penumbra was determined by quantitative immunoblot analysis. In focal cerebral ischemia, eNOS expression increased significantly to 129%+/-6% of the value for sham-operated controls (n=4, P<0.01). In contrast, AQP4 expression decreased significantly to 52%+/-3% of the value for shamoperated controls (n=4, P<0.01). These findings suggest that the expression of eNOS and AQP4 in the focal cerebral ischemia may play different roles in the formation of vasogenic brain edema. Additionally, a larger decrease in the neuronal nuclei (NeuN) (39%+/-7% of the value in sham-operated controls; n=4, P<0.01) than the decrease in glial fibrillary acidic protein (GFAP) (53%+/-14% of sham-operated controls; n=4, P<0.01) in the penumbra after focal cerebral ischemia suggests that the neurons are more susceptible to ischemic injury than are the astrocytes.

Keyword

Brain edema; Focal cerebral ischemia; eNOS; AQP4

MeSH Terms

Astrocytes
Brain
Brain Edema
Brain Injuries
Brain Ischemia
Edema
Glial Fibrillary Acidic Protein
Intracranial Pressure
Neurons
Nitric Oxide Synthase Type III
Glial Fibrillary Acidic Protein
Nitric Oxide Synthase Type III