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

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

Ke-Xuan Liu, PhD MD^*,, Timo Rinne, PhD MD, Wei He, PhD MD, Fang Wang, MD MSc and Zhengyuan Xia, PhD, MD

^* From the Department of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China; the
Anesthesiology Research Laboratory, Department of Anesthesiology, Renmin Hospital, Wuhan University, Wuhan, Hubei, China; the
Division of Cardiac Anesthesia and Intensive Care, Heart Center, Tampere University Hospital, Tampere, Finland; and the
Department of Anesthesiology, Guangdong Provincial People’s Hospital, Guangzhou, China.

Address correspondence to: Dr. Ke-Xuan Liu, Dept. of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. E-mail: liukexuan807{at}yahoo.com.cn. Or to: Dr. Zhengyuan Xia, Anesthesiology Research Laboratory, Dept. of Anesthesiology, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuhan, 430060, China. Phone: +86 27 88041919; Fax: +86 27 88042292; E-mail: zhengyuan_xia{at}yahoo.com. Current address: University of Calgary, Dept of Pharmacology & Therapeutics, Calgary, Alberta, Canada.

Purpose: 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·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.

Conclusion: 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.