Dexmedetomidine did not reduce the effects of tourniquet‐induced ischemia‐reperfusion injury during general anesthesia

Abstract

Ischemia reperfusion injury causes the release of free oxygen radicals. Free oxygen radicals initiate the production of toxic metabolites, such as malondialdehyde (MDA), through the lipid peroxidation of cellular membranes. Following lipid peroxidation, the antioxidant enzyme system is activated against reactive oxygen species (ROS) and attempts to protect cells from oxidative damage. There is a balance between the scavenging capacity of antioxidant enzymes and ROS. Because of this balance, the total antioxidant capacity (TAC) measurement is a sensitive indicator of the overall protective effects of the antioxidants. Alpha(2) receptor agonists are effective in preventing hemodynamic reactions during extremity surgeries by preventing the release of catecholamines secondary to tourniquet application. They have also been shown to possess preventive effects in various ischemia-reperfusion injury models. In our study, we examined the effects of dexmedetomidine on tourniquet-induced ischemia-reperfusion injury in lower extremity surgeries performed under general anesthesia. The effects of dexmedetomidine were measured with serum MDA and TAC levels. We studied 60 adult American Society of Anesthesiologists (ASA) physical status I or II patients undergoing one-sided lower extremity surgery with tourniquet. The patients were randomly divided into two groups. Group D was administered a dexmedetomidine infusion at a rate of 0.1μg/kg/minute(-1) for 10 minutes prior to induction and then at 0.7μg/kg/hour(-1) until 10 minutes before the end of the operation. The control group (Group C) received a saline infusion of the same amount and for the same period of time. General anesthesia was induced with thiopental, fentanyl, and rocuronium and maintained with nitrous oxide and sevoflurane in both groups. Venous blood samples were obtained before the administration of the study drugs (basal) at 1 minute before tourniquet release and at 5 and 20 minutes after tourniquet release (ATR). In both groups, MDA levels decreased at 5 and 20 minutes ATR when compared with the basal values (p<0.05). TAC levels decreased at 1 and 5 minutes ATR and then returned to basal values at 20 minutes ATR (p<0.05). In reference to the prevention of lipid peroxidation in tourniquet-induced ischemia-reperfusion injury, the results from the two groups in our study showed that dexmedetomidine did not have an additional protective role during routine general anesthesia.

The Effect of Intravenous Anesthetics on Ischemia-Reperfusion Injury

“…The main findings of the study demonstrated that serum MDA levels were decreased when compared to basal values at 5 and 20 minutes ATR and that TAC was lower than basal values at 1 minute before and at 5 minutes ATR and reached the basal level at 20 minutes ATR. However, these findings were similar to the results obtained from the group that was not given dexmedetomidine [20]. …”

Curcumin and dexmedetomidine prevents oxidative stress and renal injury in hind limb ischemia/reperfusion injury in a rat model

“…41 On the other hand, in another study in lower extremity surgeries Dex was found to be ineffective in reducing the effects of tourniquet-induced ischemia-reperfusion injury during general anesthesia. 42 Studies focusing on the renoprotective effects of Dex have gained popularity in recent years but their effects are shown to be eliminated by a2-adrenoreceptor antagonists. Several mechanisms of renoprotection, have suggested including cytoprotective effect in extracellular regulated protein kinases (ERK) signaling pathway and suppressing the activation of JAK2/STAT3 signaling pathway.…”

Role of Intravenous Dexmedetomidine in Prolonging Postoperative Analgesia and Quality of Block Following Spinal Anaesthesia. A Systemic Review and Update

“…One study has demonstrated that use of dexmedetomidine in post-bypass period in coronary bypass surgery had lower incidence of acute kidney injury [84]. Few other animal experimental study has shown organ protective effects of dexmedetomidine on myocardial protection [82,85] neuronal protection in spinal cord injury [86][87][88][89], reduction in cerebral vasospasm after sub-arachnoid haemorrhage, [89] prevention of retinal apoptosis in retinal ischaemia [90], preventive effects in Acute lung injury [91], visceral and renal protection in ischemic-repurfusion injury [81][82][83][84]92,93]. The ability to protect against organ dysfunction, notably myocardial, renal and neuronal, may yet to be the defining characteristic of this class of drug in human being.…”