The effects of increasing PGE2 on translocation of labeled albumin into rat brain

Under pathophysiological conditions, infiltration of leukocyte plays a key role in the progression of the neuroinflammatory reaction in the CNS. Prostaglandin E(2) (PGE(2)) is known to accumulate at lesion sites of the post-ischemic brain. Although post-ischemic treatments with cyclooxygenase-2 inhibitors reduce blood-brain barrier (BBB) leukocyte infiltration, the direct effect of PGE(2) on BBB has not been fully implemented. Therefore, the direct effect of increasing PGE(2) infusion on translocation of labeled albumin into the brain was assessed. Under anesthesia rats were drilled stereo-taxicaly a burr hole in the right forebrain and PGE(2) was infused into the forebrain and the hole was occluded. The animals were then injected with fluorescent labeled albumin (FA), via internal right jugular vein and decapitated at different infusion time points. The forebrain was removed and each forebrain hemisphere was homogenized and fluorescence intensities were measured in the supernatant. The fluorescence intensities measured in the right and left forebrain hemispheres of the control group (0.0 μg PGE(2)) were almost identical. Four hours after infusion of PGE(2) at doses higher than 250 μg, fluorescence intensity increased in the right forebrain supernatant, even if it was not statistically significant. The fluorescence intensity was detectable in the brain supernatant 4 h after infusion of PGE(2) in doses higher than 250 μg PGE(2.) The highest fluorescence intensity was 16 h after infusion of 500 μg PGE(2), which returned to near control values after 48 h. Increased fluorescence intensity in the brain following PGE(2) infusion is concluded to be associated with disruption of the BBB.