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Article: Effect of methylprednisolone on reperfusion injury in severe oncontrolled hemorrhagic shock

TitleEffect of methylprednisolone on reperfusion injury in severe oncontrolled hemorrhagic shock
Authors
KeywordsHemorrhagic
Lipid peroxidation
Methylprednisolone
Reperfusion injury
Shock
Issue Date2003
Citation
Chinese Journal Of Traumatology - English Edition, 2003, v. 6 n. 6, p. 359-362 How to Cite?
AbstractObjective: To study the effect of methylprednisolone (MP) on reperfusion injury in severe uncontrolled hemorrhagic shock and explore the possible mechanism involved. Methods: Twelve dogs were randomly divided into two groups, control group (Group I, n = 6) and MP group (Group II, n = 6). The animals were bled continuously from a femoral artery catheter to produce uncontrolled hemorrhagic shock models. Resuscitation with lactated Ringer's (LR) solution was initiated when mean arterial pressure (MAP) decreased to 20 mm Hg, and MAP was maintained at 30-40 mm Hg. MP (4 mg/kg) was injected intravenously in Group II when resuscitation began. While in Group I, normal saline (NS) was injected instead. The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) were measured before exsanguination (T1), when MAP decreased to 20 mm Hg (T2), 60 min (T3) and 120 min (T4) after resuscitation. Heart rate, MAP and cardiac output (CO) levels were recorded concomitantly. Results: Infusion volume and hemorrhage volume shed from the superior mesenteric artery in Group I were higher than those in Group II (P < 0.01 and P < 0.05). After reperfusion, blood SOD levels decreased progressively and MDA levels increased rapidly in Group I. In Group II, blood SOD levels at T3 and T4 decreased as compared with that at T1 but a stepwise increase was present. At T4, blood SOD level was significantly higher in Group II than in Group I (P < 0.01). At T3 and T4, MDA levels were markedly lower in Group II than in Group I. During reperfusion, MAP was more steady in Group II than in Group I and survival rate after 120 min (at T4) was higher in Group II than in Group I (P < 0.05). Conclusions: MP has a protective effect on severe uncontrolled hemorrhagic shock and subsequent reperfusion injury. The mechanism mainly involves the anti-lipid peroxidation activity of MP.
Persistent Identifierhttp://hdl.handle.net/10722/147206
ISSN
2020 SCImago Journal Rankings: 0.442
References

 

DC FieldValueLanguage
dc.contributor.authorXia, Fen_US
dc.contributor.authorCao, JSen_US
dc.contributor.authorZhan, LYen_US
dc.contributor.authorXia, ZYen_US
dc.contributor.authorXia, ZYen_US
dc.contributor.authorHuang, HBen_US
dc.date.accessioned2012-05-29T06:00:47Z-
dc.date.available2012-05-29T06:00:47Z-
dc.date.issued2003en_US
dc.identifier.citationChinese Journal Of Traumatology - English Edition, 2003, v. 6 n. 6, p. 359-362en_US
dc.identifier.issn1008-1275en_US
dc.identifier.urihttp://hdl.handle.net/10722/147206-
dc.description.abstractObjective: To study the effect of methylprednisolone (MP) on reperfusion injury in severe uncontrolled hemorrhagic shock and explore the possible mechanism involved. Methods: Twelve dogs were randomly divided into two groups, control group (Group I, n = 6) and MP group (Group II, n = 6). The animals were bled continuously from a femoral artery catheter to produce uncontrolled hemorrhagic shock models. Resuscitation with lactated Ringer's (LR) solution was initiated when mean arterial pressure (MAP) decreased to 20 mm Hg, and MAP was maintained at 30-40 mm Hg. MP (4 mg/kg) was injected intravenously in Group II when resuscitation began. While in Group I, normal saline (NS) was injected instead. The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) were measured before exsanguination (T1), when MAP decreased to 20 mm Hg (T2), 60 min (T3) and 120 min (T4) after resuscitation. Heart rate, MAP and cardiac output (CO) levels were recorded concomitantly. Results: Infusion volume and hemorrhage volume shed from the superior mesenteric artery in Group I were higher than those in Group II (P < 0.01 and P < 0.05). After reperfusion, blood SOD levels decreased progressively and MDA levels increased rapidly in Group I. In Group II, blood SOD levels at T3 and T4 decreased as compared with that at T1 but a stepwise increase was present. At T4, blood SOD level was significantly higher in Group II than in Group I (P < 0.01). At T3 and T4, MDA levels were markedly lower in Group II than in Group I. During reperfusion, MAP was more steady in Group II than in Group I and survival rate after 120 min (at T4) was higher in Group II than in Group I (P < 0.05). Conclusions: MP has a protective effect on severe uncontrolled hemorrhagic shock and subsequent reperfusion injury. The mechanism mainly involves the anti-lipid peroxidation activity of MP.en_US
dc.languageengen_US
dc.relation.ispartofChinese Journal of Traumatology - English Editionen_US
dc.subjectHemorrhagic-
dc.subjectLipid peroxidation-
dc.subjectMethylprednisolone-
dc.subjectReperfusion injury-
dc.subjectShock-
dc.subject.meshAnalysis Of Varianceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshDrug Administration Scheduleen_US
dc.subject.meshFemaleen_US
dc.subject.meshLipid Peroxidationen_US
dc.subject.meshMaleen_US
dc.subject.meshMethylprednisolone - Pharmacologyen_US
dc.subject.meshProbabilityen_US
dc.subject.meshRandom Allocationen_US
dc.subject.meshReference Valuesen_US
dc.subject.meshReperfusion Injury - Drug Therapy - Physiopathologyen_US
dc.subject.meshSensitivity And Specificityen_US
dc.subject.meshShock, Hemorrhagic - Drug Therapy - Physiopathologyen_US
dc.subject.meshSurvival Rateen_US
dc.titleEffect of methylprednisolone on reperfusion injury in severe oncontrolled hemorrhagic shocken_US
dc.typeArticleen_US
dc.identifier.emailXia, ZY:zyxia@hkucc.hku.hken_US
dc.identifier.authorityXia, ZY=rp00532en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid14642057-
dc.identifier.scopuseid_2-s2.0-0345169803en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0345169803&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume6en_US
dc.identifier.issue6en_US
dc.identifier.spage359en_US
dc.identifier.epage362en_US
dc.publisher.placeChinaen_US
dc.identifier.issnl1008-1275-

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