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KMID : 0371319940470061004
Journal of the Korean Surgical Society
1994 Volume.47 No. 6 p.1004 ~ p.1010
Octreotide and Ischemia Injury of the Small Intesine
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Abstract
To evaluate whether Octreotide acetate (OA, somatostatin analogue) could suppress the injury effect of the gastrointestinal contents on the bowel with pre-existing ischemia injury, weanling male rats with diverted loop were utilized. With
pre-treatment
of aminophylline(40mg/kg), superior, mesenteric artery was clamped for 15 minutes. After 30 minutes of reperfusion, aa specimen(30-min) was taken. A segment of mid-small bowel, 10cm long, was diverted as Thiry-Vella loop with restoration of the
continuity of remaining intestine to allow regular feeding later on. OA(2 ug/kg) was given subcutaneously to group II(N=8) and same amount of saline to group I(N=8) in 8 hours interval for 32 hours from the immediate post-operation. After 48
hours
of
reperfusion with oral feeding, one specimen from the diverted loop(D-loop) and another from main intestinal tract(M-tract) were taken for histomorphometric examinations, such as villus size ratio(VSR, height divided by width of each villus),
injury
score(IS) and crypt size (CS, depth of crypt) to evaluate the preserving status, the severity of the mucosal injury and the mucosal regeneration of each bowel, respecively.
VSR of M-tract was higher in group II(2.5¡¾0.9) than that in group I(2.1¡¾0.8). But there was no difference of VSR in D-loop between each group. IS of M-tract and D-loop were in group II (15.3¡¾3.5, 8.3¡¾1.9) than those in group I(29.5¡¾3.6,
13.6¡¾4.5).
CS of D-loop(13.3¡¾3.0, 10.3¡¾2.8) were larger than those of 30-min(7.2¡¾2.1, 6.9¡¾1.7) and of M-tract(7.2¡¾2.0, 6.9¡¾1.9) in group I and II, respectively. And CS of D-loop in group II(10.3¡¾2.8) decreased more than that of group I (13.3¡¾3.0),
which
means suppression of the mucosal regeneration after ischemia injury. These results suggest that OA could attenuate the additive injury by gastrointestinal contents to the ischemic bowel. In addition, OA might have direct cytoprotection on the
mucosa
rather than stimulation of mucosal regeneration under these circumstances.
KEYWORD
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