Abstract

The effects of intravenous anesthetics on ischemia-reperfusion injury (IRI) have been investigated in both animals and clinical studies. The protective effects and the dosages of the intravenous anesthetics on IRI were discussed in this paper. The prevention of the tissue injury after the IRI was demonstrated with intravenous anesthetics in some studies. In the future, the studies should be focused on the dosage of the anesthetics related to diminishing the tissue injuries. Further studies might be required in order to investigate the effects of the anesthetics on molecular levels.

Highlights

  • Ischemia-reperfusion injury (IRI) can be resulted from many factors such as the release of free oxygen radicals and consecutive lipid peroxidation, cell death by apoptosis or necrosis, inflammatory cytokines, and damage to the microvasculature [1, 2]

  • Thorough understanding of the pathophysiology of liver IRI may yield novel therapeutic strategies to reduce IRI and lead to improved clinical outcomes [3]. Both experimental and clinical studies focusing on the reduction of IRI report that tissue injury may be prevented through the use of anesthetic agents or anesthesia methods

  • A continuous infusion of dexmedetomidine (1 μg/kg for 10 minutes, followed by 0.5 μg/kg h−1) was used until the end of surgery, whereas the control group received an equivalent volume of saline. Their results suggest that dexmedetomidine may offer advantages by inhibiting lipid peroxidation in the case of anticipated ischemia-reperfusion injury, which would occur in upper-extremity surgery requiring tourniquet application [19]

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Summary

Introduction

Ischemia-reperfusion injury (IRI) can be resulted from many factors such as the release of free oxygen radicals and consecutive lipid peroxidation, cell death by apoptosis or necrosis, inflammatory cytokines, and damage to the microvasculature [1, 2]. The results of the study indicated that remifentanil postconditioning protected the heart from ischemia-reperfusion injury to a similar extent as of ischemic postconditioning This protection involves κ and δ but not μ opioid receptor activation [13]. The cardioprotective effects of IV-administered fentanyl using a model of myocardial ischemia-reperfusion injury associated with pharmacologically induced central sympathetic over activity were investigated. A continuous infusion of dexmedetomidine (1 μg/kg for 10 minutes, followed by 0.5 μg/kg h−1) was used until the end of surgery, whereas the control group received an equivalent volume of saline Their results suggest that dexmedetomidine may offer advantages by inhibiting lipid peroxidation in the case of anticipated ischemia-reperfusion injury, which would occur in upper-extremity surgery requiring tourniquet application [19]. Hypertension following the administration of high-dose dexmedetomidine is associated with cerebral hypoperfusion and the exacerbation of ischemic brain injury, possibly through alpha-2-induced cerebral vasoconstriction [21]

Propofol
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Ketamine
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