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Protective effects of amlodipine on ischemia-reperfusion injury of rat ovary: biochemical and histopathologic evaluation.
Fertility and Sterility 2008 December
OBJECTIVE: To evaluate the effects of amlodipine as an antioxidant and analyze the histopathologic changes in experimental ischemic and ischemic-reperfusion (I/R) injury in rat ovaries.
DESIGN: Experimental study.
SETTING: Experimental surgery laboratory.
ANIMAL(S): Forty-two rats with experimentally induced ovarian torsion.
INTERVENTION(S): Group 1: sham operation; group 2: bilateral ovarian ischemia; group 3: 3-hour period of ischemia plus 3 hours of reperfusion; groups 4 and 5: amlodipine administration at 3 and 5 mg/kg respectively before one half hour of ischemia, and then bilateral ovarian ischemia. The ovaries were removed at the third hour of ischemia. Groups 6 and 7: 3-hour period of bilateral ovarian ischemia. Two and a half hours after the induction of ischemia, the rats received amlodipine. At the end of a 3-hour period of ischemia, 3 hours of reperfusion was continued; then the ovaries were removed.
MAIN OUTCOME MEASURE(S): Ovarian tissue superoxide dismutase and nitric oxide activity; histopathologic examination of all ovarian rat tissue.
RESULT(S): Ischemia and I/R increased the inducible nitric oxide synthase activity while decreasing the superoxide dismutase activity significantly in comparison with the sham group. Both doses of amlodipine before ischemia and I/R reversed the trend in nitric oxide synthase activities and reversed the trend in the rat's ovary.
CONCLUSION(S): Conservative treatment with amlodipine is effective in reducing tissue damage induced by ischemia, I/R, or both in ovaries.
DESIGN: Experimental study.
SETTING: Experimental surgery laboratory.
ANIMAL(S): Forty-two rats with experimentally induced ovarian torsion.
INTERVENTION(S): Group 1: sham operation; group 2: bilateral ovarian ischemia; group 3: 3-hour period of ischemia plus 3 hours of reperfusion; groups 4 and 5: amlodipine administration at 3 and 5 mg/kg respectively before one half hour of ischemia, and then bilateral ovarian ischemia. The ovaries were removed at the third hour of ischemia. Groups 6 and 7: 3-hour period of bilateral ovarian ischemia. Two and a half hours after the induction of ischemia, the rats received amlodipine. At the end of a 3-hour period of ischemia, 3 hours of reperfusion was continued; then the ovaries were removed.
MAIN OUTCOME MEASURE(S): Ovarian tissue superoxide dismutase and nitric oxide activity; histopathologic examination of all ovarian rat tissue.
RESULT(S): Ischemia and I/R increased the inducible nitric oxide synthase activity while decreasing the superoxide dismutase activity significantly in comparison with the sham group. Both doses of amlodipine before ischemia and I/R reversed the trend in nitric oxide synthase activities and reversed the trend in the rat's ovary.
CONCLUSION(S): Conservative treatment with amlodipine is effective in reducing tissue damage induced by ischemia, I/R, or both in ovaries.
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