Con: Ischemic preconditioning is not necessary because volatile agents accomplish it

Abstract

ISCHEMIC PRECONDITIONING (IPC) is an endogenous protection against prolonged ischemia. It has been described as a short ischemia before a sustained ischemia.1 This sublethal ischemia triggers underlying protective biochemical mechanisms involving adenosine, protein kinase C, tyrosine kinase, free oxygen radical production, and activation of mitochondrial and/or sarcolemmal adenosine triphosphate-sensitive potassium (KATP) channels opening.2 Several other triggers of preconditioning have been described, such as hypoxia, thermal stress, pacing, or stretch. Pharmacologic agents are also able to mimic IPC with similar results; these agents include adenosine, acetylcholine, bradykinin, angiotensin, alpha-receptor agonists, or KATP channel openers. In addition, currently available anesthetic agents are also able to mimic preconditioning.3,4 Opioids5 and all volatile halogenated anesthetics6 can protect the heart against ischemia when administrated before ischemia. Both IPC and anesthetic preconditioning (APC) present 2 temporal windows of preconditioning: an early phase lasting for only 1 to 2 hours and a second late phase, occurring between 12 and 72 hours after a preconditioning stimulus, which involves new protein synthesis such as nitric oxide synthases, heat stress proteins, antioxidant enzyme systems, and cyclooxygenase-2. IPC and APC share similar mechanisms, with slight differences.7 Reduction in infarct size occurs with a similar magnitude by ischemic or anesthetic preconditioning.8 IPC was demonstrated in 1986 in an experimental animal model1 and in humans during cardiopulmonary bypass in 1993.9