Protective Effects And Mechanisms Of Propofol On Myocardium Ischemia/Reperfusion Injury In Rats

Myocardium ischemia-reperfusion injury is a commonly occurred perioperative cardiac problem. Several pathogenic mechanisms have been proposed to explain the myocardial damage that occurs during myocardium ischemia- reperfusion injury. In recent years, Oxidative stress has been shown to play a pivotal role in the pathogenesis of ischemia-reperfusion injury. Apoptosis (programmed cell death) is the cellular basis in oxidative stress induced by ischemia/reperfusion injury. Mitochondria as oxidative stress sensor and death signal integrator play a key role in initiating and mediating apoptosis of cardiomyocytes suffered from ischemia/reperfusion damage.It has been shown that most inhalational anesthetics such as isoflurane, enflurane, sevoflurane could protect the myocardium against ischemia reperfusion injury, reduce the infarct volume and ameliorate myocardial function. The mechanisms of inhalational anesthetics preconditioning have been widely investigated. KATP and PKC have been proposed as important mediators of inhalational anesthetic-induced cardioprotection.Propofol, 2,6-diisopropylphenol, an intravenous anaesthetic with a rapid and short anesthesia, is frequently used during cardiac surgery and in postoperative sedation. There are reports that propofol can protect myocardium against the ischemia/reperfusion in isolated rat hearts .It has been proposed that this action of propofol may be mediated by its ability to act as a free radical scavenger conferred by the phenolichydroxyl group in its structure or through inhibition of trans-membrane calcium channels. However, Coetzee reported that propofol failed to protect the pig heart suffered from ischemia reperfusion injury induced by left anterior descending coronary artery occlusion. So the protective effects against myocardial ischemia/reperfusion injury provided by propofol are not known and the mechanisms for the...