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

TitlePropofol attenuates intestinal mucosa injury induced by intestinal ischemia-reperfusion in the rat
Authors
Issue Date2007
PublisherCanadian Anesthesiologists' Society. The Journal's web site is located at http://www.cja-jca.org/
Citation
Canadian Journal Of Anesthesia, 2007, v. 54 n. 5, p. 366-374 How to Cite?
AbstractPurpose: 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 enclothelin-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 malondialclehyde (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.
Persistent Identifierhttp://hdl.handle.net/10722/147245
ISSN
2015 Impact Factor: 2.139
2015 SCImago Journal Rankings: 0.884
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLiu, KXen_US
dc.contributor.authorRinne, Ten_US
dc.contributor.authorHe, Wen_US
dc.contributor.authorWang, Fen_US
dc.contributor.authorXia, Zen_US
dc.date.accessioned2012-05-29T06:01:00Z-
dc.date.available2012-05-29T06:01:00Z-
dc.date.issued2007en_US
dc.identifier.citationCanadian Journal Of Anesthesia, 2007, v. 54 n. 5, p. 366-374en_US
dc.identifier.issn0832-610Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/147245-
dc.description.abstractPurpose: 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 enclothelin-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 malondialclehyde (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.en_US
dc.languageengen_US
dc.publisherCanadian Anesthesiologists' Society. The Journal's web site is located at http://www.cja-jca.org/en_US
dc.relation.ispartofCanadian Journal of Anesthesiaen_US
dc.subject.meshAnimalsen_US
dc.subject.meshEndothelin-1 - Analysisen_US
dc.subject.meshFree Radical Scavengers - Therapeutic Useen_US
dc.subject.meshIntestinal Mucosa - Drug Effects - Pathology - Ultrastructureen_US
dc.subject.meshIntestine, Small - Blood Supply - Metabolismen_US
dc.subject.meshLactic Acid - Analysisen_US
dc.subject.meshMaleen_US
dc.subject.meshMalondialdehyde - Analysisen_US
dc.subject.meshNitric Oxide - Analysis - Metabolismen_US
dc.subject.meshPropofol - Therapeutic Useen_US
dc.subject.meshRandom Allocationen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshReperfusion Injury - Metabolism - Prevention & Controlen_US
dc.subject.meshSeverity Of Illness Indexen_US
dc.subject.meshSuperoxide Dismutase - Metabolismen_US
dc.titlePropofol attenuates intestinal mucosa injury induced by intestinal ischemia-reperfusion in the raten_US
dc.typeArticleen_US
dc.identifier.emailXia, Z:zyxia@hkucc.hku.hken_US
dc.identifier.authorityXia, Z=rp00532en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid17470888-
dc.identifier.scopuseid_2-s2.0-34250205286en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34250205286&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume54en_US
dc.identifier.issue5en_US
dc.identifier.spage366en_US
dc.identifier.epage374en_US
dc.identifier.isiWOS:000246329600007-
dc.publisher.placeCanadaen_US

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