Hostname: page-component-745bb68f8f-g4j75 Total loading time: 0 Render date: 2025-01-11T12:54:05.040Z Has data issue: false hasContentIssue false
  • English
  • Français

The effects of sevoflurane and desflurane on lipid peroxidation during laparoscopic cholecystectomy

Published online by Cambridge University Press:  23 December 2004

G. M. Koksal ,
C. Sayilgan ,
S. Aydin ,
H. Uzun  and
H. Oz
G. M. Koksal
Affiliation:
Istanbul University Cerrahpasa Medical Faculty, Departments of Anaesthesiology and Reanimation, Istanbul, Turkey
C. Sayilgan
Affiliation:
Istanbul University Cerrahpasa Medical Faculty, Departments of Anaesthesiology and Reanimation, Istanbul, Turkey
S. Aydin
Affiliation:
Istanbul University Cerrahpasa Medical Faculty, Department of Biochemistry, Istanbul, Turkey
H. Uzun
Affiliation:
Istanbul University Cerrahpasa Medical Faculty, Department of Biochemistry, Istanbul, Turkey
H. Oz
Affiliation:
Istanbul University Cerrahpasa Medical Faculty, Departments of Anaesthesiology and Reanimation, Istanbul, Turkey
Get access

Abstract

Summary

Background and objective: To compare the effects of sevoflurane and desflurane anaesthesia on lipid peroxidation.

Methods: We studied 40 healthy patients undergoing elective laparoscopic cholecystectomy. Patients were randomly allocated to be anaesthetized either with sevoflurane (n = 20) or desflurane (n = 20). Anaesthesia was maintained with inspiratory concentrations of sevoflurane 1–1.5 MAC (n = 20) or desflurane (n = 20). Samples were taken for plasma malondialdehyde and superoxide dismutase assays before induction of anaesthesia, before skin incision and at the end of surgery. Alveolar cell samples were obtained from the lungs using the technique of protective blind bronchoalveolar lavage, after induction of anaesthesia and at the end of surgery for malondialdehyde and superoxide dismutase concentrations.

Results: Plasma malondialdehyde increased more after the administration of desflurane than after sevoflurane: after induction 5.9 ± 0.6 nmol mL−1 for desflurane vs. 3.8 ± 0.5 nmol L−1 for sevoflurane (P < 0.001); at the end of the surgery: 6.7 ± 0.4 nmol mL−1 for desflurane vs. 4.2 ± 0.3 nmol mL−1 for sevoflurane (P < 0.001). There was a small but significant increase in plasma superoxide dismutase concentration after desflurane – from 24.2 ± 1.2 to 24.9 ± 0.9U mL−1 after induction and 25 ± 1U mL−1 at the end of the surgery (P < 0.01) but no increase with sevoflurane. Malondialdehyde concentrations increased significantly in the cells obtained by protective blind bronchoalveolar lavage at the end of surgery in the desflurane group (from 0.3 ± 0.1 to 1.7 ± 0.2 nmol mL−1 (P < 0.001)), but not in the sevoflurane group. There were no significant differences between the two anaesthetics in the amounts of superoxide dismutase in the samples obtained by protective blind bronchoalveolar lavage.

Conclusions: Desflurane may cause more systemic and regional lipid peroxidation than sevoflurane during laparoscopic cholecystectomy in healthy human beings.

Keywords

ALDEHYDES, malondialdehyde, thiobarbituric acid reactive substancesANAESTHETICS INHALATION, desflurane, sevofluraneENERGY METABOLISM, oxidation–reduction, lipid peroxidationENZYMES, oxidoreductases, superoxide dismutaseINVESTIGATIVE TECHNIQUES, irrigation, bronchoalveolar lavage
Type
Original Article
Information
European Journal of Anaesthesiology , Volume 21 , Issue 3 , March 2004 , pp. 217 - 220
Copyright
2004 European Society of Anaesthesiology

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Goode HF, Cowley HC, Walker BE, Howdle PD, Webster NR. Decreased antioxidant status and increased lipid peroxidation in patients with septic shock and secondary organ dysfunction. Crit Care Med 1995; 23: 646–651.Google Scholar
Kotani N, Lin CY, Wang JS, et al. Loss of alveolar macrophages during anaesthesia and operation in humans. Anesth Analg 1995; 81: 1255–1262.Google Scholar
Halliwell B, Gutteridge JMC, Cross CE. Free radicals, antioxidants and human disease: where are we now? J Lab Clin Med 1992; 119: 598–600.Google Scholar
Mercer RR, Russell ML, Roggli VL, Crapo JD. Cell number and distribution in human and rat airways. Am J Respir Cell Mol Biol 1994; 10: 613–624.Google Scholar
McCord JM. The evaluation of free radicals and oxidative stress. Am J Med 2000; 108: 652–659.Google Scholar
Rouby JJ, Rossignon MD, Nicholas MH. A prospective study of protected bronchoalveolar lavage in the diagnosis of nasocomial pneumonia. Anesthesiology 1989; 71: 679–685.Google Scholar
Angel MF, Ramasastry SS, Swartz WM, et al. The critical relationship between free radicals and degrees of ischemia: evidence for tissue intolerance of marginal perfusion. Plastic Reconstruct Surg 1988; 81: 233–259.Google Scholar
Sun Y, Oberley LW, Li Y. A simple method for clinical assay of superoxide dismutase. Clin Chem 1988; 3413: 497–500.Google Scholar
Haga Y, Beppu T, Doi K, et al. Systemic inflammatory response syndrome and organ dysfunction following gastrointestinal surgery. Crit Care Med 1997; 25: 1994–2000.Google Scholar
Suter PM, Ricov B. Cytokines and lung injury. In: Marini JJ, Evans TW, eds. Acute Lung Injury. Berlin, Germany: Springer-Verlag, 1998: 41–53.
Wrigge H, Zinserling J, Stüber F, et al. Effects of mechanical ventilation on release of cytokines into systemic circulation in patients with normal pulmonary function. Anesthesiology 2000; 93: 1413–1417.Google Scholar
Kotani N, Takahaski S, Sessler DI, et al. Volatile anesthetics augment expression of proinflammatory cytokines in rat alveolar macrophages during mechanical ventilation. Anesthesiology 1999; 91: 187–197.Google Scholar
Douglas RG, Shaw JHF. Metabolic response to sepsis and trauma. Br J Surg 1989; 76: 115–122.Google Scholar
Stahl W. Acute phase protein response to tissue injury. Crit Care Med 1987; 15: 545–550.Google Scholar
Allaouchiche B, Debon R, Goudable J, Chassard D, Duflo F. Oxidative stress status during exposure to propofol, sevoflurane and desflurane. Anesth Analg 2001; 93: 981–985.Google Scholar
De Groot H, Noll T. Halothane-induced lipid peroxidation and glucose-6-phosphatase inactivation in microsomes under hypoxic conditions. Anesthesiology 1985; 62: 42–48.Google Scholar
National Research Council (USA). In: Bunker JP, Forest WH, Mosteller H, et al. National Halothane Study: A Study of the Possible Association between Halothane Anesthesia and Postoperative Hepatic Necrosis. Washington DC, USA: Government Printing Office, 1969.
Frink E, Brown B. Sevoflurane. Anaesth Pharmacol Rev 1994; 2: 61–67.Google Scholar
Mogil'nitskaia LV, Prokof'ev VN, An F, Zhogolev VV. The effect of hypoxia on membrane status and lipid peroxidation in rat lungs and blood. Vopr Med Khim 1993; 39: 34–36.Google Scholar
Boya P, de la Pena A, Beloqui O, et al. Antioxidant status and glutathione metabolism in prepheral blood mononuclear cells from patients with chronic hepatitis C. J Hepatol 1999; 31: 808–814.Google Scholar
Eger IIEl, Johnson BH, Ferrell LD. Comparison of the toxicity of I-653 and isoflurane in rats: a test of the effect of repeated anesthesia and use of dry soda lime. Anesth Analg 1987; 66: 1230–1233.Google Scholar