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.

Effect of Kineret® on ovarian ischemia reperfusion injury in a rat model

“…Numerous studies have reported a decrease in tGSH levels in ovarian IR injury. 26,27 GSH, which is an endogenous antioxidant consisting of glutamate, cysteine and glycine, protects cells from oxidative damage created by free oxygen radicals. 28 Consistent with the literature, our results revealed that the oxidant/antioxidant balance changed in favor of oxidants in the ovarian tissue of rats subjected to IR.…”

Molecular targets and mechanism of action of dexmedetomidine in treatment of ischemia/reperfusion injury (Review)

“…Glutathione is involved in DNA synthesis and repair, cellular metabolic functions, inactivation of toxic substances and the prevention of damage caused by free radicals (49). In rats, the increased reliance of spinal α 2 -ARs on cholinergic stimulation to cause analgesia following nerve injury reflects, in part, a shift from direct inhibition to direct excitation of spinal cholinergic neurons, which, in turn, depends on brain-derived neurotrophic factors and on an interaction with the stimulatory G protein (50).…”

The Preventive Effect of Dexmedetomidine Against Postoperative Intra-abdominal Adhesions in Rats

“…MDA is the end product of lipid peroxidation and is widely used as a marker of oxidative activity. 33 In a study by Kurt et al, 34 the inhibition of acute I/R damage by dexmedetomidine in rat ovarian tissue was investigated, and microscopic findings, such as very severe edema, very severe vascular congestion, hemorrhage and leukocytic infiltrates, were found to be present in the ovarian tissue with elevated MDA; these histologic observations indicated that the increase in MDA was related to the intensity of the tissue injury. Gideroglu et al 35 also reported that ischemic insult resulted in high MDA levels in an inferior epigastric artery skin flap as a flap I/R injury model.…”