Infarct-remodeled Myocardium Is Receptive to Protection by Isoflurane Postconditioning

Abstract

Infarct-remodeled myocardium is receptive to protection by isoflurane postconditioning via protein kinase B/Akt signaling. This is the first time to demonstrate that anesthetic postconditioning retains its marked protection in diseased myocardium.

Caveolin-3 expression and caveolae are required for isoflurane-induced cardiac protection from hypoxia and ischemia/reperfusion injury

“…Isoflurane administration can activate opioid and adenosine receptors and blockade of these G-protein-coupled receptors can abolish cardiac protection produced by isoflurane [30]. Volatile anesthetics affect several signaling pathways implicated in preconditioning, including Src tyrosine kinase (Src), the phosphatidylinositol-3-kinase(PI3K)/protein kinase B/glycogen synthase kinase 3 beta pathway [31], protein kinase C (PKC) [32,33], and mitogen-activated protein kinases (MAPK), including extracellular signal-regulated kinase 1 and 2 (ERK1/2) [34] and p38 MAPK [35]. In addition, volatile anesthetics modulate ATP-sensitive potassium channel activity [32,33], the generation of reactive oxygen species, and mitochondrial permeability transition pore opening [36].…”

Sevoflurane Postconditioning Protects Chronically-Infarcted Rat Hearts against Ischemia-Reperfusion Injury by Activation of Pro-survival Kinases and Inhibition of Mitochondrial Permeability Transition Pore Opening upon Reperfusion

“…[10][11][12] At the end of the experiments, hearts were frozen at Ϫ20°C for 2 h and subsequently cut into five cross-section slices. Heart slices were incubated in a 1% TTC in 0.1 M phosphate buffer solution (pH 7.4) at 37°C for 20 min, and fixed overnight in 10% formaldehyde.…”

“…[10][11][12] In brief, ligation of the LAD coronary artery was performed in penbarbital-anesthetized rats, which were orally intubated and mechanically ventilated. Left thoracotomy was performed by opening the fourth intercostal space.…”

Cardioprotection Techniques: Preconditioning, Postconditioning and Remote Con-ditioning (Basic Science)

“…Our laboratory and others have demonstrated that the cardioprotective benefits of IPost are dependent on the activation of Akt and Erk1/2 at the immediate onset of myocardial reperfusion [213,214]. Subsequent studies have confirmed the role for Akt and Erk1/2 in the setting of IPost in both non-diseased animal hearts and diseased ones [215,216] as well as human atrial muscle [217]. Interestingly, obese mice have been reported to be resistant to IPost protection, and this finding was associated with insufficient activation of the RISK pathway in the hearts harvested from obese animals compared to control ones [218].…”