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Am J Physiol Gastrointest Liver Physiol 276: G1174-G1180, 1999;
0193-1857/99 $5.00
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Vol. 276, Issue 5, G1174-G1180, May 1999

Experimental colitis increases blood-brain barrier permeability in rabbits

Christopher A. Hathaway, Caroline B. Appleyard, William H. Percy, and John L. Williams

Department of Physiology and Pharmacology, School of Medicine, The University of South Dakota, Vermillion, South Dakota 57069

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 × 10-5 ml/s and 0.48 × 10-5 ± 0.13 × 10-5 ml/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 × 10-5 ml/s, n = 7) compared with untreated controls (0.19 × 10-5 ± 0.04 × 10-5 ml/s, n = 8). PS product for fluorescein increased (P < 0.01) in HAc colitis compared with vehicle (2.66 × 10-5 ± 1.46 × 10-5 ml/s and 0.33 × 10-5 ± 0.05 × 10-5 ml/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.

cerebral blood flow; brain-gut axis; colitis model; inflammatory bowel disease; vasculature


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