Halici Zekai, Karaca Mehmet, Keles Osman Nuri, Borekci Bunyamin, Odabasoglu Fehmi, Suleyman Halis, Cadirci Elif, Bayir Yasin, Unal Bunyami
Department of Pharmacology, Ataturk University School of Medicine, Erzurum, Turkey.
Fertil Steril. 2008 Dec;90(6):2408-15. doi: 10.1016/j.fertnstert.2007.10.007. Epub 2008 Feb 21.
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.
Experimental study.
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.
评估氨氯地平作为抗氧化剂的作用，并分析大鼠卵巢实验性缺血及缺血再灌注（I/R）损伤中的组织病理学变化。
实验研究。
实验外科实验室。
42只实验性诱导卵巢扭转的大鼠。
第1组：假手术；第2组：双侧卵巢缺血；第3组：3小时缺血加3小时再灌注；第4组和第5组：在缺血前半小时分别给予3和5mg/kg氨氯地平，然后进行双侧卵巢缺血。在缺血第3小时取出卵巢。第6组和第7组：双侧卵巢缺血3小时。缺血诱导后2.5小时，大鼠接受氨氯地平。在3小时缺血结束时，继续进行3小时再灌注；然后取出卵巢。
卵巢组织超氧化物歧化酶和一氧化氮活性；所有大鼠卵巢组织的组织病理学检查。
与假手术组相比，缺血和I/R显著增加诱导型一氧化氮合酶活性，同时降低超氧化物歧化酶活性。缺血和I/R前的两种剂量氨氯地平均逆转了一氧化氮合酶活性的趋势，并逆转了大鼠卵巢中的趋势。
氨氯地平保守治疗对减轻卵巢缺血、I/R或两者所致的组织损伤有效。
