The effect of acute stress exposure on ischemia and reperfusion injury in rat heart: Role of oxytocin

  title={The effect of acute stress exposure on ischemia and reperfusion injury in rat heart: Role of oxytocin},
  author={Maryam Moghimian and Mahdieh Faghihi and Seyed Morteza Karimian and Alireza Imani},
  pages={385 - 392}
Previous studies showed the protective effects of oxytocin (OT) on myocardial injury in ischemic and reperfused rat heart. Moreover, exposure to various stressors not only evokes sudden cardiovascular effects but also triggers the release of OT in the rat. The present study was aimed to evaluate the possible cardioprotective effects of endogenous OT released in response to stress (St), and effects of administration of exogenous OT on the ischemic–reperfused isolated heart of rats previously… 

Upregulated Hsp27 expression in the cardioprotection induced by acute stress and oxytocin in ischemic reperfused hearts of the rat.

It is suggested that endogenous OT may participate in stress-induced cardioprotection via Hsp27 over-expression as an early response.

Contribution of upregulated Hsps expression to the cardioprotection effect of oxytocin released in acute stress in ischemic reperfused hearts of the rat

Findings suggest that preconditio ning effect of oxytocin at the periphery released in response to a cute stress may be via Hsp27 over-expression as an early warning sign in stressinduced cardioprotection of heat shock proteins.

Could nitric oxide be a mediator of action of oxytocin on myocardial injury in rats? (Biochemical, histological and immunohistochemical study).

It is concluded that OT has antioxidant, anti-inflammatory and anti-apoptotic effects on MI and its effects is mediated through NO.

Prolonged oxytocin treatment in rats affects intracellular signaling and induces myocardial protection against infarction.

Positive effects of oxytocin that may ameliorate negative consequences of stress on the heart are, at least in part, mediated through p38-MAPK and Akt kinase pathways.

Evaluation of Chronic Physical and Psychological Stress Induction on Cardiac Ischemia / Reperfusion Injuries in Isolated Male Rat Heart: The Role of Sympathetic Nervous System.

Results show that induction of chronic physical and psychological stress prior to ischemia/reperfusion causes enhancement of myocardial injuries and it seems that increased sympathetic activity in response to stress is responsible for these adverse effects of stress on ischemic/ reperfused heart.

Acute Physical Stress Preconditions the Heart Against Ischemia/Reperfusion Injury Through Activation of Sympathetic Nervous System

Findings indicate that acute physical stress can act as a preconditional stimulator and probably, the presence of sympathetic nervous system is necessary.



Biphasic protective effect of oxytocin on cardiac ischemia/reperfusion injury in anaesthetized rats

The protective effect of oxytocin on renal ischemia/reperfusion injury in rats

Oxytocin exerts protective effects on in vitro myocardial injury induced by ischemia and reperfusion.

The data suggest that the negative chronotropic action of oxytocin participates in its protective effects on ischemia-reperfusion-induced myocardial injury, and demonstrates an attenuation of the infarct size in oxytocIn-treated hearts, indicating a cardioprotective effect of Oxytocin.

Repeated physiologic stresses provide persistent cardioprotection against ischemia-reperfusion injury in rats.

Effect Of Different Doses Of Noradrenaline Against Ischemia-induced Ventricular Arrhythmias In Rat Heart In Vivo

Noradrenaline dose-dependently attenuated ischemia-induced ventricular arrhythmias in open chest anesthetized rats and significantly attenuated severity and incidence of arrh rhythmias.

Repeated intermittent stress exacerbates myocardial ischemia-reperfusion injury.

Experimental evidence corroborating correlative studies in humans that link chronic stress with increased morbidity and mortality from ischemic heart disease is provided.

Omega 3 has a beneficial effect on ischemia/reperfusion injury, but cannot reverse the effect of stressful forced exercise.

Infarct size‐reducing effect of heat stress and α1 adrenoceptors in rats

Both α1A and α1B adrenoceptor subtypes appear to play a role in the heat stress‐induced cardioprotection, independently of the HSP72 level, and further investigations are required to elucidate the precise role of HSPs in this adaptative response.