Persistance et voie de l’inhibition de la production de superoxyde par les neutrophiles induite par isoflurane

Abstract

Background Our previous work has demonstrated that treatment with isoflurane has a preconditioning-like inhibitory effect on superoxide production (SOP) by polymorphonuclear neutrophils. The current objectives were to determine persistency of this effect and to clarify where in the signalling pathway this inhibition of SOP occurred. The latter was accomplished using two receptor-dependent neutrophil agonists, platelet activating factor (PAF) and formyl-methionyl-leucyl-phenylalanine (fMLP), and two receptor-independent neutrophil stimuli, the protein-kinase C stimulator, phorbol myristate acetate (PMA), and the calcium ionophore, A23187.Methods Arterial blood samples were obtained from eight dogs under baseline condition (conscious state), during isoflurane (1 MAC) administration, and 24 and 48 hr post-isoflurane (also in conscious state). Neutrophils were isolated and stimulated with 1 lM concentrations of PAF, fMLP, PMA, and A23187. SOP was measured spectrophotometrically. Results Isoflurane administration caused (1) an approximate 50% decrease in SOP during PAF or fMLP (P \ 0.01 vs baseline), which remained evident from 24 to 48 hr following isoflurane; (2) an initial 29% decrease in SOP during PMA (P \ 0.05 vs baseline), which returned to baseline by 24 hr following isoflurane; and (3) no change in SOP during A23187 (P [ 0.05 vs baseline). Conclusions Isoflurane administration caused prolonged (from 24 to 48 hr) decreases in agonist-induced SOP by neutrophils. This effect involved inhibition at site(s)

Subanesthetic Isoflurane Reduces Zymosan-Induced Inflammation in Murine Kupffer Cells by Inhibiting ROS-Activated p38 MAPK/NF-κB Signaling

“…However, clinically relevant doses of ISO protect organs (e.g., lung, liver, kidney, and intestine) injury induced by inflammation resulting from endotoxemia or ischemia-reperfusion [42–46]. Moreover, 1.4% ISO administration causes prolonged decreases in agonist-induced superoxide production by neutrophils [47]. These conflicting findings possibly stemmed from different pathological states or molecular mechanisms employed by ISO.…”

Sevoflurane inhibits equine myeloperoxidase release and activity in vitro

“…In addition, halogenated anaesthetics attenuate the production of ROS by activated PMN (Frohlich et al. 1997; Saad et al. 2010).…”

“…(1997) demonstrated that the volatile anaesthetics halothane, enflurane and sevoflurane inhibited the oxidative response of human neutrophils to fMLP challenge by inhibiting the signal transduction upstream of protein kinase C (PKC), possibly at the level of the calcium‐calmodulin complex. In a concordant study, Saad et al. (2010) used receptor‐dependent and receptor‐independent stimuli to show that isoflurane decreased PMNs respiratory burst by inhibition of the signalling pathway upstream from PKC.…”

“…Indeed, volatile anaesthetics have been shown to preserve endothelial integrity (Chappell et al 2011) and reduce the expression of adhesion molecules on endothelium and neutrophils (de Rossi et al 2002) thus limiting PMNs accumulation in inflamed tissues. In addition, halogenated anaesthetics attenuate the production of ROS by activated PMN (Frohlich et al 1997;Saad et al 2010). Taking together these effects, halogenated anaesthetics may reduce organ dysfunction during inflammatory stress (Hu et al 2003).…”

Impact of Anesthetics on Immune Functions in a Rat Model of Vagus Nerve Stimulation

“…However, isoflurane can potentially interfere at different levels, such as the central nervous system [9], [10] or the immune system. Indeed, isoflurane has anti-inflammatory properties which can be sources of interferences in studies concerning inflammation [11], [12], [13], [14], [15], [16], [17], [18]. Moreover, the use of isoflurane has not yet been studied in a VNS rat model.…”