Effect of isoflurane preconditioning on gut injury following intestinal ischemia-reperfusion in rats / 中国药学杂志

ABSTRACT

OBJECTIVE: To observe the effect of isoflurane of different concentrations on the intestinal ischemia-reperfusion injury (IRI) in rats, and to preliminarily investigate its mechanism. METHODS: Sixty adult male SD rats (200-220 g) were randomly divided into five groups (n=12 in each group) sham operation group (sham group), intestinal ischemia-reperfusion group (IRI group), and isoflurane precondition for 30 min groups (0.25M group, 0.5M group, 1.0M group). Carotid artery was cannulated for mean arterial blood pressure (MAP) monitoring every 30 min during the experiment. Two hours after reperfusion, 3 mL of blood were collected from the inferior cava, which was centrifugated to test the activity of SOD, the contents of MDA and TNF-α. And a strip of small intestine was taken from the distal end of ileum for preparation of pathology HE staining sections which were observed for the structural damage under microscope and quantitatively assessed the damage degree by improved Chiu's scale. Meanwhile, the expression of protein caspase-3 was analyzed by immunohistochemical and Western Blot methods. RESULTS: Compared with IRI, the MAP of isoflurane APC group was significantly improved. The improved Chiu's scales in 0.5M group and 1.0M group were obviously lower than that in IRI group, but there was no significant difference between 0.25 M group and IRI group (P > 0.05). The plasma SOD activity in IRI group was lower than sham group (P 0.05), but signif icantly decreased in 0.5M group (P < 0.01). Compared with IRI group and 0.25M group, the protein expression of Caspase-3 in 0.5M group and 1.0M group was reduced significantly (P < 0.05). CONCLUSION: Isoflurane preconditioning at 0.5 MAC and 1.0MAC for 30 min can similarly protect against the intestinal IRI, but 0.25MAC isoflurane has little protective effect. The protective effect of isoflurane against acute intestinal IRI is probably by improving the activity of SOD, reducing the lipid peroxidation, and inhibiting the cell apoptosis and TNF-α-induced inflammation cascade.