Canadian Journal of Anesthesia

, Volume 54, Issue 5, pp 366–374

Propofol attenuates intestinal mucosa injury induced by intestinal ischemia-reperfusion in the rat

Reports of Original Investigations



We investigated whether propofol at a sedative dose can prevent intestinal mucosa ischemia/reperfusion (I/R) injury, and if propofol can attenuate oxidative stress and increases in nitric oxide (NO) and endothelin-1 (ET-1) release that may occur during intestinal I/R injury.


Rats were randomly allocated into one of five groups (n=10 each): (i) sham control; (ii) injury (one hour superior mesenteric artery occlusion followed by three hours reperfusion); (iii) propofol pre-treatment, with propofol given 30 min before inducing intestinal ischemia; (iv) simultaneous propofol treatment, with propofol given 30 min before intestinal reperfusion was started; (v) propofol post-treatment, with propofol given 30 min after intestinal reperfusion was initiated. In the treatment groups, propofol 50 mg·kg−1 was administrated intraperitoneally. Animals in the control and untreated injury groups received equal volumes of intralipid (the vehicle solution of propofol) intraperitoneally. Intestinal mucosa histology was analyzed by Chiu’s scoring assessment. Levels of lactic acid (LD), NO, ET-1, lipid peroxidation product malondialdehyde (MDA) and superoxide dismutase (SOD) activity in intestinal mucosa were determined.


Histological results showed severe damage in the intestinal mucosa of the injury group accompanied by increases in MDA, NO and ET-1 and a decrease in SOD activity. Propofol treatments, especially pre-treatment, significantly reduced Chiu’s scores and levels of MDA, NO, ET-1 and LD, while restoring SOD activity.


These findings indicate that propofol attenuates intestinal I/R-induced mucosal injury in an animal model. The response may be attributable to propofol’s antioxidant properties, and the effects of inhibiting over-production of NO and in decreasing ET-1 levels.

Le propofol atténue les lésions de la muqueuse intestinale provoquées par l’ischémie-reperfusion intestinale chez le rat



Nous avons cherché à savoir si le propofol, en dose sédative, pouvait empêcher les lésions d’ischémie/reperfusion (I/R) de la muqueuse intestinale, et s’il pouvait atténuer le stress oxydatifet les augmentations dans la libération d’oxyde nitrique (NO) et d’endothéline-1 (ET-1) pouvant survenir lors de lésions I/R intestinales.


Des rats ont été randomisés en cinq groupes (n = 10 chacun) : (i) faux témoin (sham control) ; (ii) lésion (occlusion de l’artère mésentérique supérieure d’une heure suivie par reperfusion de trois heures) ; (iii) prétraitement au propofol, avec administration de propofol 30 min avant de provoquer l’ischémie intestinale ; (iv) traitement simultané au propofol, avec administration de propofol 30 min avant le début de la reperfusion intestinale ; (v) traitement ultérieur au propofol, avec administration de propofol 30 min après le début de la reperfusion intestinale. Dans les groupes de traitement, du propofol a été administré en dose intrapéritonéale de 50 mg·kg−1. Les animaux des groupes témoin et lésions nontraitées ont reçu des volumes équivalents d’Intralipid (la solution véhicule du propofol) en dose intrapéritonéale. L’histologie de la muqueuse intestinale a été analysée par l’évaluation des points de Chiu (Chiu’s scoring assessment). Les niveaux d’acide lactique (LD), NO, ET-1, l’activité de produits de péroxydation lipidique de malondialdéhyde (MDA) et de superoxyde dismutase (SOD) dans la muqueuse intestinale ont été déterminés.


Les résultats histologiques ont montré des lésions graves de la muqueuse intestinale dans le groupe lésions, accompagnées d’une augmentation de MDA, NO et ET-1 et une diminution de l’activité SOD. Les traitements au propofol, particulièrement le prétraitement, ont réduit de façon significative les résultats et niveaux de MDA, NO, ET-1 et LD sur l’échelle de Chiu, tout en restaurant l’activité SOD.


Ces résultats indiquent que le propofol atténue les lésions de la muqueuse intestinale provoquée par I/R chez le modèle animal. La réaction peut être attribuée aux propriétés anti-oxydantes du propofol, ainsi qu’aux effets d’inhibition de la surproduction de NO et de la diminution des niveaux de ET-1.


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Copyright information

© Canadian Anesthesiologists 2007

Authors and Affiliations

  1. 1.Department of AnesthesiologyThe First Affiliated Hospital, Sun Yat-sen UniversityGuangzhouChina
  2. 2.Anesthesiology Research Laboratory, Department of AnesthesiologyRenmin Hospital, Wuhan UniversityWuhanChina
  3. 3.Division of Cardiac Anesthesia and Intensive CareHeart Center, Tampere University HospitalTampereFinland
  4. 4.Department of AnesthesiologyGuangdong Provincial People’s HospitalGuangzhouChina
  5. 5.Dept of Pharmacology & TherapeuticsUniversity of CalgaryCalgaryCanada

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