Superoxide dismutase (SOD) exogenously administered has been documented to protect gastric mucosa against ischemia-reinfusion injury by scavenging oxygen radicals. However, the changes in levels of endogenous SOD in ischemic gastric mucosa are not known. To evaluate this, the present study was designed.
Methods: Fasted and anesthetized SD rats were given 0.1 N HCl i.g. and received the following procedures. Study 1: (1) Ischemia group--25 min after acid instillation, blood pressure was reduced to 20-30 mmHg for 20 min. (2) Ischemia-Reinfusion group--5 min after acid administration, rats received the same hypotension as above followed by reinfusion of shed blood for 20 min. (3) Control group-Rats were killed 45 min later without hypotension and reinfusion. Study 2: Three groups of rats treated with the same procedures as in Study 1 were given allopurinol (50 mg/kg/day) i.g. once daily for 2 days prior to the experiment. All rats were killed by exsanguination from the carotid artery to avoid as much as possible contamination of gastric mucosal samples with red blood cells rich in SOD. The supernatants of the corpus and antral mucosa homogenized were prepared for measuring their SOD activity using the nitrite method modified by Oyanagui.
Results: SOD activity in the gastric mucosa significantly increased in both the Ischemia (Ische.) and Ischemia-Reinfusion (I-R) groups compared to the control (Ische. vs. I-R vs. Cont'l: corpus-123.4 +/- 4.8 vs. 127.4 +/- 3.6 vs. 96.9 +/- 4.4 NU/Mg protein; antrum-71.6 +/- 2.8 vs. 81.4 +/- 6.8 vs. 62.1 +/- 3.1 NU/mg protein). No increase in SOD activity was observed in rats pretreated with allopurinol.
Conclusion: SOD activity increases with oxyradicals generation in the rat stomach subjected to either hemorrhagic ischemia alone or hemorrhagic ischemia plus reinfusion. This also suggests that oxyradicals are generated even in the ischemic period.