title: Propofol attenuates intestinal mucosa injury induced by intestinal ischemia-reperfusion in the rat.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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 x 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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. liukexuan807@yahoo.com.cn
authors.forename: Ke-Xuan
authors.initials: KX
authors.lastname: Liu
authors.forename: Timo
authors.initials: T
authors.lastname: Rinne
authors.forename: Wei
authors.initials: W
authors.lastname: He
authors.forename: Fang
authors.initials: F
authors.lastname: Wang
authors.forename: Zhengyuan
authors.initials: Z
authors.lastname: Xia
mesh_terms: D000818:Animals; D019332:Endothelin-1 / Q000032:analysis; D016166:Free Radical Scavengers / Q000627:therapeutic use*; D007413:Intestinal Mucosa / Q000187:drug effects* / Q000473:pathology / Q000648:ultrastructure; D007421:Intestine, Small / Q000098:blood supply* / Q000378:metabolism; D019344:Lactic Acid / Q000032:analysis; D008297:Male; D008315:Malondialdehyde / Q000032:analysis; D009569:Nitric Oxide / Q000032:analysis / Q000378:metabolism; D015742:Propofol / Q000627:therapeutic use*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*; D012720:Severity of Illness Index; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D019332:Endothelin-1; D016166:Free Radical Scavengers; D009569:Nitric Oxide; D019344:Lactic Acid; D008315:Malondialdehyde; D013482:Superoxide Dismutase; D015742:Propofol