Evaluation of the effects of hyperbaric oxygen treatment and enoxaparin on left colon anastomosis. An experimental study.

BACKGROUND: Surgical interventions on left colon lead to high morbidity. The problems in wound healing are the main cause of this morbidity. Hypoxia retards wound healing and hyperbaric oxygen treatment (HBOT) has an anti-hypoxic effect. MATERIALS AND METHODS: In this experimental study we divided eighty Wistar albino rats into eight groups and numbered between 1 and 8. Normal (non-ischemic) and ischemic left colon anastomosis were performed in the first and second four groups respectively. HBOT and subcutaneous enoxaparin were applied to the groups separately and in combination for four days, except the control groups. (Group-1 and Group-5). We measured anastomotic bursting pressures and performed pathological examinations besides electron microscopic study in one sample from each group after sacrificing the rats on the fourth day. RESULTS: There were no statistically significant differences in bursting pressures when we compared Group-1 with other non-ischemic groups, and Group-5 with Group-6, but there were statistically significant differences when we compared Group-5 with Group-7 and 8. In pathological examination, there were no statistically significant differences between the groups concerning necrosis, epithelization, granulation tissue formation and collagen deposition. Statistically significant differences were found in the scores of neovascularization when we compared Group-1 with Group-3 and 4, and Group-5 with Group-8. Electron microscopic evaluation revealed a prominent increase both in neovascularization and collagen fibers in the samples taken from the groups received enoxaparine and hyperbaric oxygen treatment in combination. CONCLUSIONS: These findings suggest that HBOT increases neovascularization and bursting pressures in ischemic colon anastomosis in contrast with enoxaparin.

Ebselen as protection against ethanol-induced toxicity in rat stomach.

The mucosal protective effect of ebselen was examined in an ethanol-induced rat gastric lesion model. Examination of gastric tissue samples by light microscopy showed that i.g. exposure to 50% ethanol induced gastric injury, which was more prominent in female rats. Ethanol did not effect the gastric acid secretion examined by means of H(+)-K+ATPase, the increment of which might be harmful in the stomach. But ebselen with or without ethanol kept H(+)-K+ATPase below control levels. Gastric alcohol dehydrogenase (ADH) was mainly responsible for oxidation of ethanol in the stomach before it enters the bloodstream. I.g. ethanol exposure inhibited the ADH activity but ebselen eliminated the ethanol-induced inhibition of this enzyme. Therefore, ebselen exhibited a beneficial effect by increasing the gastric ethanol metabolism and by ameliorating the possible tissue toxicity of ethanol. Consistently, we also found that ebselen diminished the blood ethanol level. A gender difference in the blood ethanol levels existed following the same dose of ethanol but there was no difference in ADH activity. Histologically, mucosal injury following ebselen exposure together with ethanol was less severe compared with ethanol treatment alone. We concluded that the decrease in ethanol-induced mucosal injury following ebselen may have contributed to the inhibition of H(+)-K+ATPase and the activation of ADH by ebselen.

Nitric oxide-mediated regulation of gastric H+, K+ -ATPase and alcohol dehydrogenase following ethanol-induced injury in rats.

The mucosal protective effect of nitric oxide (NO) was examined by using N(G)-nitro-L-arginine methyl ester (L-NAME) as nitric oxide synthase (NOS) inhibitor and nitroprusside (NP) as NO donating agent, in ethanol-induced rat gastric lesion model. The results are summarized as follows: (1) As gastric tissue samples were examined by light microscopy, intragastric exposure of ethanol was demonstrated to induce gastric injury, which was more prominent in female rats. The depletion of NO by L-NAME treatment exacerbated the ethanol-induced gastric lesion but NP together with ethanol promoted repair of the mucosal injury, especially in female rats. (2) Gastric H+, K+ -ATPase enzyme activity, which was responsible for acid secretion, seemed not to be effected by ethanol treatment. Together with ethanol, L-NAME treatment activated, whereas NP treatment inhibited, the enzyme activity in female rats. (3) Ethanol treatment inhibited gastric alcohol dehydrogenase (ADH) activity, which was responsible for the first-pass metabolism of ethanol. Together with ethanol, L-NAME did not effect the enzyme activity whereas NP treatment disappeared the inhibitory effect of ethanol in both gender. Hydroxyl radical (OH*) scavenger activity was found to increase in ethanol and ethanol + NP groups in both sexes, but superoxide radical (O2-*) scavenger activity did not change. The results indicate that NO may ameliorate the damaging effect of ethanol possibly by regulating acid secretion, ethanol metabolism, and antioxidant content in rat gastric mucosa.