Cardioprotection with halogenated gases: how does it occur?

Abstract

Numerous studies have studied the effect of halogenated agents on the myocardium, highlighting the beneficial cardiac effect of the pharmacological mechanism (preconditioning and postconditioning) when employed before and after ischemia in patients with ischemic heart disease. Anesthetic preconditioning is related to the dose-dependent signal, while the degree of protection is related to the concentration of the administered drug and the duration of the administration itself. Triggers for postconditioning and preconditioning might have numerous pathways in common; mitochondrial protection and a decrease in inflammatory mediators could be the major biochemical elements. Several pathways have been identified, including attenuation of NFκB activation and reduced expression of TNFα, IL-1, intracellular adhesion molecules, eNOS, the hypercontraction reduction that follows reperfusion, and antiapoptotic activating kinases (Akt, ERK1/2). It appears that the preconditioning and postconditioning triggers have numerous similar paths. The key biochemical elements are protection of the mitochondria and reduction in inflammatory mediators, both of which are developed in various ways. We have studied this issue, and have published several articles on cardioprotection with halogenated gases. Our results confirm greater cardioprotection through myocardial preconditioning in patients anesthetized with sevoflurane compared with propofol, with decreasing levels of troponin and N-terminal brain natriuretic peptide prohormone. The difference between our studies and previous studies lies in the use of sedation with sevoflurane in the postoperative period. The results could be related to a prolonged effect, in addition to preconditioning and postconditioning, which could enhance the cardioprotective effect of sevoflurane in the postoperative period. With this review, we aim to clarify the importance of various mechanisms involved in preconditioning and postconditioning with halogenated gases, as supported by our studies.

Assessing the influence of isoflurane anesthesia on cardiac metabolism using hyperpolarized [1‐13C]pyruvate

“…The impact of isoflurane on cardiac metabolism has been examined in the context of ‘anesthetic preconditioning’, where multiple underlying molecular mechanisms modulating cardiac metabolism have been identified . Isoflurane acts on mitochondrial membranes, activating potassium channels and indirectly attenuating oxidative phosphorylation .…”

Conflicting Actions of Inhalational Anesthetics, Neurotoxicity and Neuroprotection, Mediated by the Unfolded Protein Response

“…This integrated form of stress response is involved in a variety of pathological conditions [58,59]. Other research has shown that during anesthesia for cardiac surgery, inhalational anesthetics produce similar effects as those induced by ischemia [60]. Thus, sevoflurane has been used as a clinically beneficial agent for anesthetic preconditioning, or pharmacological preconditioning [61].…”

Assessing the optimal preparation strategy to minimize the variability of cardiac pyruvate dehydrogenase flux measurements with hyperpolarized MRS

“…For example, levels of circulating FAs may modulate PDH flux . Isoflurane anaesthesia, as used in this study, has also been shown to attenuate mitochondrial oxidative phosphorylation and glycolytic flux, which modulates cardiac PDH flux detectable by hyperpolarized [1‐ 13 C] pyruvate MRS . We used a constant supply of 2% isoflurane in medical oxygen throughout all our experiments, although there may be variable sensitivity to the anaesthetic gas in our cohort, especially if the rats have different amounts of fat deposits.…”