Abstracts
1999 Digestive Disease Week

# 4673 NEW INSIGHTS INTO THE IMPAIRMENTOF MUCOSAL DEFENSE IN PORTAL HYPERTENSIVE GASTRIC MUCOSA
M Tomikawa, Y Akiba, J D Kaunitz, H Kawanaka, K Sugimachi, A S Tarnawski, I James Sarfeh, VA Med Ctr, Long Beach, CA

Portal hypertention (PHT) increases susceptibility of the gastric mucosa to injury. We previously reported that PHT induces changes in gastric microvasculature and increases gastric permability to luminal acid (Hepatology 1988; 8: 1488-1494). The aim of this study was to investigate whether PHT affects rat gastric mucosal defense mechanisms in vivo at the pre-epithelial, epithelial and/or post-epithelial levels. METHODS: PHT was produced in rats by staged portal vein ligation. Sham operated rats served as controls. Fourteen days after the operations, the gastric mucosa was exposed, chambered and continuously superfused with buffers under microscopy. We used novel techniques to determine gastric mucosal gel layer thickness, surface mucous cell intracellular pH (pHi), and gastric mucosal blood flow and oxygenation in vivo. STUDIES: 1) Gastric mucosal gel layer thickness measurements in vivo by a re-focussing technique; 2) Surface mucous cell pHi using an in vivo microfluorometric technique; 3) Gastric mucosal blood flow measurement with laser Doppler flowmetry; 4)Gastric mucosal and serosal oxygenation with an oxygen sensor. RESULTS: 1) Gastric mucosal gel layer thickness was significantly reduced in PHT rats compared with controls (88.2±16.1 mm in PHT rats vs.135.0±24.7 mm in controls, p<0.0001). 2) Baseline gastric surface mucous cell pHi was significantly decreased in PHT rats (6.80±0.11 in PHT rats vs. 7.09±0.21 in controls; p<0.01). 3) Total gastric mucosal blood flow was significantly increased in PHT rats (67.6±45.3 PU rats vs 39.4±14.0 PU, p<0.05). 4) Oxygenation of the gastric mucosal but not serosal surface in PHT rats was decreased by 42% (p<0.05). CONCLUSIONS: 1) PHT impairs pre-epithelial (mucosal gel layer thickness) and epithelial (pHi), components of the gastric mucosal barrier. 2) While overall gastric blood flow is increased in PHT rats, maldistribution of blood flow (post-epithelial component) is probably the cause of impaired mucosal surface oxygenation. These findings can explain the increased susceptibility of portal hypertensive gastric mucosa to injury.

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