Sıçanlarda intestinal iskemi-reperfüzyon hasarında oksitosin tedavisinin sonuçları

Abstract

Ischemia-reperfusion injury is a clinical condition that poses a life-threatening risk due to certain diseases or operations such as trauma, shock, and gastric dilatation volvulus. The study's objective was to investigate the impact of oxytocin on intestinal damage in rats caused by ischemia-reperfusion injury induced experimentally. Three groups of Wistar albino rats were formed: Control (CTR, n=6), intestinal ischemia-reperfusion (I-IR, n=6), and intestinal ischemia-reperfusion+ Oxytocin (I-IR+Oxt, n=6). Oxytocin (1 mg/kg) was given intraperitoneally to the I-IR+Oxt group 30 min prior to the anesthesia. In the I-IR and I-IR+Oxt groups, ischemia reperfusion was performed with 1 h ligation of the superior mesenteric artery and one hour reperfusion by opening the ligatures. After the end of the reperfusion period, euthanasia was performed and blood and intestinal tissue samples were taken. From the blood samples, ALT, ALP, AST, LDH, BUN, creatinine, IL-1β, TNF-α, concentrations and from the tissue sample, IL-1β, TNF-α and MDA activities were evaluated. While serum and tissue IL-1β, TNF-α concentrations were greater in both I-IR and I-IR+Oxt groups compared to the CTR group, these levels were determined to be lower in the I-IR+Oxt group compared to the I-IR group. Histopathological analysis showed that epithelial regeneration of both epithelium and glands structure and decreased inflammatory cell infiltration were found in the I-IR+Oxt group compared to the I-I/R group. In conclusion, oxytocin inhibited the release of IL-1β and TNF-α and the harmful effect of IR on intestinal cells.