1995 Fiscal Year Final Research Report Summary
DEVELOPMENT AND REPAIR OF MICRO-INJURY IN GASTRIC MUCOSA
| Project/Area Number |
06670570
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | NAGOYA CITY UNIVERSITY |
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Principal Investigator |
JOH Takashi NAGOYA CITY UNIVERSITY,MEDICAL SCHOOL ASSISTANT PROFESSOR, 医学部, 助手 (30231369)
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| Co-Investigator(Kenkyū-buntansha) |
ITOH Makoto NAGOYA CITY UNIVERSITY,MEDICAL SCHOOL ASSOCIATE PROFESSOR, 医学部, 助教授 (00080119)
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| Project Period (FY) |
1994 – 1995
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| Keywords | Gastric mucosal injury / Mucosal defense / Restitution / Ischemia reperfusion / Mucosal blood flow |
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| Research Abstract |
With a support of this grant, induction and repsir of mucosal micro injury were investigated mainly in a rat model of gastric epithelial damage induced by local ischemial reperfusion (I/R), in which the damage was quantified by measuring the blood-to-lumen ^<51>Cr-EDTA clearance (Am J physiol 266 : G263-270,1994). Animal body temperature was automatically controlled and luminal perfusate was collected by a fraction collector. Using this new system, effects of stimulator of mucus production (tetraprenyl acetone ; TPA) and mucolytic agent (N-acetyl-L-cysteine ; NAC) were assessed to elucidate role of gastric mucus in I/R-induced gastric epithelial injury. The results that TPA attenuated and NAC aggravated ^<51>Cr-EDTA clearance strongly indicate a protective role of gastric mucus against I/R stress (J Lab Clin Med 126 : 287-293,1995). The role of endogenous acid was also evaluated. Proton pump inhibitor (omeprazole) or H_2-receptor antagonist (T-593) wsa used to suppress luminal acidity.
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Both drugs significantly attenuated the increase in clearance induced by I/R.However, when the luminal acid was completely neutralized by luminal perfusion with phosphate-buffered saline, no reduction in clearance was observed. These data indicate that endogenous luminal acid does not play an important role in this gastric micro injury, and that a proton pump inhibitor or H_2-receptor antagonist may suppress I/R injury by a mechanism other than reducing luminal acidity, i.e., reducing consumption of ATP needed for acid secretion to improve gastric mucosal energy metabolism (J Clin Gastroenterol 21 : S108-112,1995). In addition, the role of complement in systemic shock following intestinal ischemia was also investigated by consuming complements using cobra venom factor (CVF). Two out of 13 rats were killed by intestinal I/R.No rat was killed in CVF pretreated group. In survival animals, decrease in blood pressure was observed in I/R.CVF significantly improved this change in blood pressure. These results indicate that complements positively participate in the shock induced by intestinal I/R,and that complements might also participate in mucosal injury induced by I/R. Less
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