Increase in Antioxidant Capacity of Plasma During Propofol Anesthesia

Hans, Pol; Deby‐Dupont, G.; Deby, C.; Pieron, F.; Verbesselt, René; Franssen, Colette; Lamy, Maurice

doi:10.1097/00008506-199707000-00006

Cited by 59 publications

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“…Propofol has antioxidant actions and reduces oxidative stress. [12][13][14][15][16][17][18][19][20][21] Since propofol attenuates oxidative stress, propofol may prevent lipid peroxidation following ischemia /reperfusion in the brain. Therefore, we designed the present study using delayed neuronal death after transient forebrain ischemia in gerbils to ascertain whether propofol may prevent lipid peroxidation in the hippocampal CA1 subfield.…”

Section: Discussionmentioning

confidence: 99%

“…21 The generation of free radicals derived from oxygen after ischemia/reperfusion, which leads to the production of lipid peroxides in cell membranes, is one of the major mechanisms of tissue damage in ischemia/reperfusion. [30][31][32][33] Propofol has antioxidant properties and prevents lipid peroxidation [12][13][14][15][16][17][18][19][20][21] and has been reported to enhance tissue antioxidant capacity clinically in a few studies. 13,14,16 Propofol is similar in chemical structure to the active nucleus of the endogenous antioxidanttocopherol and butylhydroxytoluene.…”

Section: Discussionmentioning

confidence: 99%

“…[30][31][32][33] Propofol has antioxidant properties and prevents lipid peroxidation [12][13][14][15][16][17][18][19][20][21] and has been reported to enhance tissue antioxidant capacity clinically in a few studies. 13,14,16 Propofol is similar in chemical structure to the active nucleus of the endogenous antioxidanttocopherol and butylhydroxytoluene. 15,17 These molecules bind to cell membranes or to phospholipids to form free radicals, and terminate lipid peroxidation by reacting with lipid peroxyl radicals to form the nonreactive phenoxyl radical.…”

Section: Discussionmentioning

confidence: 99%

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Propofol prevents lipid peroxidation following transient forebrain ischemia in gerbils

Yamaguchi

Hamaguchi

Mishio

et al. 2000

Can J Anesth/J Can Anesth

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Purpose: To ascertain whether propofol prevents lipid peroxidation on delayed neuronal death induced by transient forebrain ischemia in the hippocampal CA1 subfield in gerbils.Methods: Forty gerbils were randomly assigned to five groups: Group I, control, sham operation treated with physiological saline solution (PSS); Group II, ischemia/reperfusion treated with PSS; Group III, ischemia/reperfusion treated with 50 mg·kg -1 propofol; Group IV, ischemia/reperfusion treated with 100 mg·kg -1 propofol; Group V, ischemia /reperfusion treated with 150 mg·kg -1 propofol. Transient forebrain ischemia was induced by occluding the bilateral common carotid arteries for four minutes under N 2 O/O 2 /halothane anesthesia after propofol or PSS. Five days later, the cerebrum was removed and each forebrain was cut into two including the hippocampus. Lipid peroxidation was determined using the production of malondialdehyde (MDA), and histopathological changes in the hippocampal CA1 subfield were examined.Results: In group II, the pyramidal cells were atrophic and pycnotic; vacuolation and structural disruption of the radial striated zone was observed. In the other four groups, these changes were not observed. Degenerative ratios of pyramidal cells were: Group I: 4.9 ± 2.3, Group II: 94.1 ± 4.5 (P < 0.01), Group III: 12.5 ± 5.7, Group IV: 11.0 ± 4.6, Group V: 9.6 ± 4.9%. Production of MDA was: Group I: 83 ± 22, Group II: 198 ± 25 (P < 0.01), Group III: 153 ± 39, Group IV: 113 ± 34, Group V: 106 ± 27 nmol·g -1 wet tissue.Conclusion: Propofol attenuated delayed neuronal death by preventing lipid peroxidation induced by transient forebrain ischemia in the hippocampal CA1 subfield in gerbils.Objectif : Vérifier si le propofol empêche la peroxydation lipidique qui survient à la mort neuronale différée induite par une ischémie transitoire du prosencéphale, dans le sous-champ CA1 de l'hippocampe chez des gerbilles.Méthode : On a réparti au hasard 40 gerbilles en cinq groupes : dans le groupe 1, témoin, elles ont subi une opération fictive traitée avec une solution physiologique salée (SPS); dans le groupe II, une ischémie/reperfusion traitée avec une SPS; dans le groupe III, une ischémie/reperfusion traitée avec 50 mg·kg -1 de propofol; dans le groupe IV, une ischémie/reperfusion traitée avec 100 mg·kg -1 de propofol et dans le groupe V, une ischémie/reperfusion traitée avec 150 mg·kg -1 de propofol. L'ischémie transitoire du cerveau antérieur a été induite par l'occlusion bilatérale des artères carotides communes pendant quatre minutes sous anesthésie au N 2 O/O 2 /halothane après l'administration de propofol ou de SPS. Cinq minutes plus tard, le cerveau a été retiré et chaque prosencéphale a été coupé en deux, incluant l'hippocampe. La peroxydation lipidique a été déterminée en utilisant la production de malondialdéhyde (MDA), et les changements histopathologiques du sous-champ CA1 de l'hippocampe ont été examinés.Résultats : Dans le groupe II, les cellules pyramidales étaient atrophiques et pycnotiques; une rupture vacuolaire et stru...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Propofol prevents lipid peroxidation following transient forebrain ischemia in gerbils

Yamaguchi

Hamaguchi

Mishio

et al. 2000

Can J Anesth/J Can Anesth

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show abstract

“…A neuromuscular blocking agent should be administered without hesitation to enable optimal airway control. Propofol may benefit treatment in early local anesthetic toxicity through a number of independent mechanisms, 96,97 including seizure suppression and antioxidant properties that may improve recovery from tissue hypoxia. However, propofol is a cardiodepressant, and its use is not advisable when there are signs of cardiac instability.…”

Section: Prevention Of Local Anesthetic Toxicitymentioning

confidence: 99%

Local anesthetic systemic toxicity

Dillane

Finucane

2010

Can J Anesth/J Can Anesth

125

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“…45 The TIVA group had less allodynia and CPTS at 3 months (38.2% v 56.5%, p ¼ 0.001) and at 6 months (33.5% v 50.6%, p ¼ 0.002). The authors theorized that this reduction in CPTS could be due to the following factors: the peripheral antinociceptive effect of propofol 42 ; the antioxidizing effects of propofol 46 ; the neuroprotective effect of propofol on injured intercostal nerves 47 ; the inhibition of NMDA subtype of glutamate receptor by propofol. 48 In addition, propofol TIVA has been shown to reduce remifentanil-induced hyperalgesia.…”

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confidence: 99%