Abstract
The volatile anesthetics protect the myocardium against ischemia/reperfusion injury when applied both before ischemia (anesthetic preconditioning) and at the onset of reperfusion (anesthetic postconditioning). Mitochondria play a central role in anesthetic pre- and postconditioning. Production of small quantities of reactive oxygen species from mitochondria and mildly acidotic mitochondrial pH induced by anesthetics are triggers for pre- and postconditioning. Furthermore, mitochondria are end effectors for various prosurvival signaling pathways. The activation of prosurvival signaling pathways with anesthetics is responsible for inhibition of mitochondrial permeability transition pore (mPTP) opening. The inhibition of mPTP opening leads to preservation of ATP synthesis, prevention of intracellular calcium accumulation and protection of myocardium.
