Experimental colitis increases blood-brain barrier permeability in rabbits

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Abstract
Extraintestinal manifestations of inflammatory bowel disease are numerous. This study examined the effects of two models of acute colitis on cerebral blood flow (CBF) and permeability of the blood-brain barrier in rabbits. CBF (measured with radiolabeled microspheres), or the extraction ratio or permeability-surface area (PS) product of the blood-brain barrier to fluorescein and FITC-dextran, was measured 48 h after colitis induction with acetic acid (HAc) or trinitrobenzene sulfonic acid (TNBS). PS product for fluorescein increased ( P < 0.05) in TNBS colitis (1.33 × 10−5 ± 0.52 × 10−5ml/s and 0.48 × 10−5 ± 0.13 × 10−5ml/s (mean ± SE) for treated ( n = 14) and untreated ( n = 10) animals, respectively. PS product for the larger FITC-dextran was not different in TNBS colitis (0.24 × 10−5 ± 0.09 × 10−5ml/s, n = 7) compared with untreated controls (0.19 × 10−5 ± 0.04 × 10−5ml/s, n = 8). PS product for fluorescein increased ( P < 0.01) in HAc colitis compared with vehicle (2.66 × 10−5 ± 1.46 × 10−5ml/s and 0.33 × 10−5 ± 0.05 × 10−5ml/s, respectively; n = 6 in each group). The extraction of fluorescein from the blood to the brain increased by 75% during TNBS colitis when compared with vehicle ( P < 0.05). CBF and cerebrovascular resistance did not change from the untreated control after TNBS colitis. Our data suggest that, irrespective of induction method, acute colitis increases the permeability of the blood-brain barrier to small molecules without changing CBF.

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