Volatile anesthetic-induced preconditioning

Abstract

The myocardium has an innate ability to protect itself from ischemic events. This protection occurs when the myocardium is exposed to a brief ischemic period prior to a more extreme ischemic event. This is termed ischemic preconditioning. Ischemic preconditioning induces a series of molecular pathways that protect the cardiac myocyte; first, for a period of 1-6 hours (early preconditioning) and, also, for a second period from 24-72 hours (delayed phase). The early preconditioning is mediated by the release of adenosine which induces a protective signal that is related to the mitochondrial KATP channel activation and activation of the δ-opioid and bradykinin receptors. The delayed phase is related to the induction of inducible nitric oxide synthase, superoxide dismutase and heat-shock proteins. Indirect evidence indicates that O2-derived free radicals are involved in the delayed phase, as noted in the early preconditioning phase. Applying ischemic preconditioning to clinical practice can be dangerous and difficult to implement in a controlled fashion. However, recent studies have shown that the use of volatile anesthetics, such as sevoflurane, isoflurane and desflurane, can mimic the early phase of ischemic preconditioning through a multi-pathway signaling of mitochondrial KATP channels. This important finding can easily be applied to clinical practice for patients undergoing surgery. It can also be significantly important for patients undergoing off-pump cardiac bypass surgery or cardiac bypass surgery where there is no cross-clamp or cardioplegia used where the probability of myocardial ischemia is greatly increased. This report will, therefore, discuss the mechanism, safety and efficacy of volatile anesthetics as inducers of cardiac preconditioning.

The “Goldilocks Zone” from a redox perspective—Adaptive vs. deleterious responses to oxidative stress in striated muscle

“…Several reviews have highlighted mechanisms involved in anesthetic-induced cardioprotection, and ROS have been commonly identified as an important element to the protective mechanism (Hu and Liu, 2009; Bonney et al, 2014; Swyers et al, 2014). ROS are known to be intricately involved in post-ischemic myocardial dysfunction and infarction, and a reduction in oxidative stress has been identified as an important component in alleviating I/R injury; (Hamilton et al, 2004; Dabkowski et al, 2008).…”

The Effect of Mitochondrial Complex I-Linked Respiration by Isoflurane Is Independent of Mitochondrial Nitric Oxide Production

“…Volatile anesthetics may trigger preconditioning, in part, by inducing the formation of ROS and reactive nitrogen species and by the release of nitric oxide (NO) [9, 10]. NO exerts a number of actions that are beneficial during myocardial ischemia-reperfusion [10, 11].…”

“…NO exerts a number of actions that are beneficial during myocardial ischemia-reperfusion [10, 11]. For example, it may act as a trigger and mediator of isoflurane-induced delayed preconditioning in rabbit myocardium [12].…”

Intrathecal l-arginine reduces the antinociception of sevoflurane in formalin-induced pain in rats

“…Peripheral stimulation can activate the Fos expression in the spinal cord. To a certain extent, the numbers of FLI neurons were directly associated with the stimulation intensity, and this has been used extensively to evaluate the analgesic efficacy of medicines [16][17][18]. In agreement with behavioral studies, intraperitoneal injection of sevoflurane caused a significant reduction in the amount of Fos-LI induced by formalin injection in the spinal cord, suggesting that sevoflurane produces antinociceptive effects partly at the spinal level.…”