Oxytocin protects rat heart against ischemia–reperfusion injury via pathway involving mitochondrial ATP-dependent potassium channel

Alizadeh, Ali Mohammad; Faghihi, Mahdieh; Sadeghipour, Hamid Reza; Mohammadghasemi, Fahimeh; Imani, Alireza; Houshmand, Fariba; Khori, Vahid

doi:10.1016/j.peptides.2010.04.012

Cited by 43 publications

(40 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[54][55][56][57][58] In addition, the anti-apoptotic effect of oxytocin in the heart and ovaries has been revealed. [51,59] However, to our knowledge, the effect of oxytocin on testicular tissues in I/R injured rat model has been reported in only one study. In an experimental study, Ghasemnezhad et al demonstrated that Johnsen scores were higher in the oxytocin-treated torsion group than in the testicular torsion group.…”

Section: Discussionmentioning

confidence: 97%

“…The effects of oxytocin on I/R have been reported in limited number of studies. [51,52] Oxytocin reduces I/R injury in rat kidney, with improved renal function, as indicated by decreased serum creatinine and BUN levels in addition to improved antioxidant status and reduced ROS. [53] Moreover, the protective effect of oxytocin on I/R injury in the liver, kidney, stomach, and urinary bladder have been reported.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Oxytocin in The Prevention of Injury Due to Testicular Torsion/Detorsion in Rats

Fırat¹,

Erdemır²,

Kölükçü³

et al. 2017

Ulus Travma Acil Cerrahi Derg

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Oxytocin in The Prevention of Injury Due to Testicular Torsion/Detorsion in Rats

Fırat¹,

Erdemır²,

Kölükçü³

et al. 2017

Ulus Travma Acil Cerrahi Derg

View full text Add to dashboard Cite

show abstract

“…In contrast, treatment with the OXY antagonist ATO elevates oxidative stress in the hearts of the newborn rats [40], abolished the cardio preconditioning effect of OXY [41], and reversed the OXY effect on gastric ischemia-reperfusion injury [42].…”

Section: Discussionmentioning

confidence: 97%

“…For the here presented study, we orientated us in the dosing regimens of previously done work in the context of OXY [8, 9, 13-15, 38, 39] and its selective OXY receptor antagonist ATO [15,[40][41][42][43]. In contrast, treatment with the OXY antagonist ATO elevates oxidative stress in the hearts of the newborn rats [40], abolished the cardio preconditioning effect of OXY [41], and reversed the OXY effect on gastric ischemia-reperfusion injury [42].…”

Section: Discussionmentioning

confidence: 99%

Oxytocin effects on experimental skin wound healing

Sorg

Grambow

Eckl

et al. 2017

Innovative Surgical Sciences

View full text Add to dashboard Cite

Objective: Oxytocin (OXY) has significant effects on mammalian behavior. Next to its role in lactation and social interactions, it is described to support better wound healing as well. However, direct OXY effects on wound healing and the regeneration of the microvascular network are still not clarified. We therefore examined the effects of OXY and an OXY receptor antagonist [atosiban (ATO)] on skin wound healing, focusing on epithelialization and neovascularization. Methods: Skin wound healing has been assessed using intravital fluorescence microscopy in a model of full dermal thickness wounds in the dorsal skin fold chamber of hairless mice. Animals received repetitive low or high doses of OXY or ATO. Morphological and cellular characterization of skin tissue repair was performed by histology and in vitro cell assays. Results: The assessment of skin tissue repair using this therapy regimen showed that OXY and ATO had no major influence on epithelialization, neovascularization, wound cellularity, or inflammation. Moreover, OXY and ATO did neither stimulate nor deteriorate keratinocyte or fibroblast migration and proliferation. Conclusion: In summary, this study is the first to demonstrate that OXY application does not impair skin wound healing or cell behavior. However, until now, the used transmitter system seems not to be clarified in detail, and it might be proposed that it is associated with the stress response of the organism to various stimuli.

show abstract

“…The opening of mitochondrial K ATP channels that have been blocked by the selective mitochondrial K ATP channel inhibiter, 5-hydroxydecanoate (5-HD), could alleviate lethal ventricular arrhythmias. Agents such as sarafotoxin 6c [10] and oxytocin [11] have been reported to inhibit ventricular arrhythmias by opening mitochondrial K ATP channels. However, whether the inhibition of arrhythmia by propofol is based on the same mechanism is unknown.…”

Section: Introductionmentioning

confidence: 99%

Effects of propofol on ischemia-induced ventricular arrhythmias and mitochondrial ATP-sensitive potassium channels

et al. 2012

View full text Add to dashboard Cite

Aim: To investigate the potential of propofol in suppressing ventricular arrhythmias and to examine whether mitochondrial ATP-sensitive potassium channels are involved. Methods: Male Sprague-Dawley rats were pretreated with intravenous infusion of propofol (Prop), a selective mitochondrial KATP channel inhibitor 5-hydroxydecanoate (5-HD), propofol plus 5-HD (Prop+5-HD), a potent mitochondrial K ATP channel opener diazoxide (DZ) or NS, respectively. The dosage of each drug was 10 mg/kg. The animals then underwent a 30 min-ligation of the left anterior descending artery. The severity of arrhythmias, the incidence of ventricular fibrillation (VF), and the time of the first run of ventricular arrhythmias were documented using an arrhythmia scoring system. Mitochondrial membrane potential (ΔΨm) was measured in freshly isolated rat cardiomyocytes with a fluorescence microscope. Results: The arrhythmia scores in the Prop and DZ group were 2.6(0-5) and 2.4(0-5), respectively, which were significantly lower than that in the control group [4.9(2-8)]. VF was not observed in both Prop and DZ groups. The first run of ventricular arrhythmias was significantly postponed in the Prop group (10.5±2.2 vs 7.3±1.9 min). Bracketing of propofol with 5-HD eliminated the anti-arrhythmic effect of propofol. In isolated rat cardiomyocytes, propofol (50 μmol/L) significantly decreased ΔΨm, but when propofol was co-administered with 5-HD, the effect on ΔΨm was reversed. Conclusion: Propofol preconditioning suppresses ischemia-induced ventricular arrhythmias in the rat heart, which are proposed to be caused by opening of mitochondrial K ATP channels.

show abstract

Oxytocin protects rat heart against ischemia–reperfusion injury via pathway involving mitochondrial ATP-dependent potassium channel

Cited by 43 publications

References 36 publications

Oxytocin in The Prevention of Injury Due to Testicular Torsion/Detorsion in Rats

Oxytocin in The Prevention of Injury Due to Testicular Torsion/Detorsion in Rats

Oxytocin effects on experimental skin wound healing

Effects of propofol on ischemia-induced ventricular arrhythmias and mitochondrial ATP-sensitive potassium channels

Contact Info

Product

Resources

About