title: An investigation about the inhibition of acute ischemia/reperfusion damage by dexmedetomidine in rat ovarian tissue.
abstract: Reperfusion has always been "the emergency intervention" to ischemic tissue. For a given period of time, tissue injury due to ischemia and reperfusion is more serious than injury due to ischemia only. Groups were as: Group 1: 25 µg/kg dexmedetomidine + ischemia/reperfusion group. Group 2: 10 mg/kg yohimbine +25 µg/kg dexmedetomidine + ischemia/reperfusion group. Group 3: Ischemia/reperfusion (control) group. Group 4: Healthy rats. Rat ovaries were exposed to a 3-hour ischemia and then reperfusion ensured for 2 hours. After ischemia/reperfusion, total glutathione, malondialdehyde, 8-hydroxyguanine levels and histopathological investigation were studied. The highest total glutathione and the lowest malondialdehyde and DNA damage levels were determined in dexmedetomidine group when compared to control group. The difference between yohimbine + dexmedetomidine and the control group was insignificant. Dexmedetomidine protects the ovarian tissue of the rat from I/R injury. It is hypothesized that this protective effect of dexmedetomidine is mediated by the α-2 adrenergic receptors. Dexmedetomidine could be useful for attenuation of tissue damage after I/R and prevention of I/R-related complications.
authors.affiliation: Department of Pathology, Education and Research Hospital, Erzurum, Turkiye.
authors.forename: Ali
authors.initials: A
authors.lastname: Kurt
authors.forename: Metin
authors.initials: M
authors.lastname: Ingec
authors.forename: Unal
authors.initials: U
authors.lastname: Isaoglu
authors.forename: Mehmet
authors.initials: M
authors.lastname: Yilmaz
authors.forename: Nihal
authors.initials: N
authors.lastname: Cetin
authors.forename: Muhammet
authors.initials: M
authors.lastname: Calik
authors.forename: Beyzagul
authors.initials: B
authors.lastname: Polat
authors.forename: Fatih
authors.initials: F
authors.lastname: Akcay
authors.forename: Cemal
authors.initials: C
authors.lastname: Gundogdu
authors.forename: Halis
authors.initials: H
authors.lastname: Suleyman
mesh_terms: D058647:Adrenergic alpha-2 Receptor Agonists / Q000737:chemistry / Q000627:therapeutic use*; D058669:Adrenergic alpha-2 Receptor Antagonists / Q000494:pharmacology; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D004249:DNA Damage / Q000187:drug effects; D020927:Dexmedetomidine / Q000037:antagonists & inhibitors / Q000627:therapeutic use*; D005260:Female; D005978:Glutathione / Q000378:metabolism; D006147:Guanine / Q000031:analogs & derivatives / Q000378:metabolism; D007511:Ischemia / Q000503:physiopathology*; D015227:Lipid Peroxidation / Q000187:drug effects; D008315:Malondialdehyde / Q000378:metabolism; D010053:Ovary / Q000098:blood supply / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D020011:Protective Agents / Q000737:chemistry / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D015016:Yohimbine / Q000494:pharmacology
chemical_list: D058647:Adrenergic alpha-2 Receptor Agonists; D058669:Adrenergic alpha-2 Receptor Antagonists; D015415:Biomarkers; D020011:Protective Agents; D015016:Yohimbine; D008315:Malondialdehyde; C024829:8-hydroxyguanine; D006147:Guanine; D020927:Dexmedetomidine; D005978:Glutathione