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Article: Revisiting ischemia and reperfusion injury as a possible cause of necrotizing enterocolitis: Role of nitric oxide and superoxide dismutase

TitleRevisiting ischemia and reperfusion injury as a possible cause of necrotizing enterocolitis: Role of nitric oxide and superoxide dismutase
Authors
KeywordsIschemia
Necrotizing enterocolitis
Reperfusion injury
Issue Date2002
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/jpedsurg
Citation
Journal Of Pediatric Surgery, 2002, v. 37 n. 6, p. 828-834 How to Cite?
AbstractBackground/Purpose: The pathogenesis of necrotizing enterocolitis (NEC) is unknown. Ischemia and reperfusion (I/R) injury has been considered a major contributing factor. Nitric oxide (NO) and superoxide dismutases (SODs) have been shown to protect bowel from I/R injury. This study aims to assess (1) the ability of premature intestine to resist I/R injury compared with mature intestine and (2) the possible role of NO and SODs in modulating such response. Methods: Intestines from 5 groups of rats (n = 6 for each study group) were studied: (1) premature, gestational age 20 days; (2) premature, gestational age 22 days; (3) full-term, newborn; (4) infant, day 15; (5) infant, day 30. Experiments: (1) The degrees of I/R injury after 0, 30, 60, 90 and 120 minutes, respectively, of ischemia and 25 minutes of I/R were assessed histologically by a pathologist who was unaware of the operative details. (2) Tissue NO and copper levels were measured by electroparamagnetic resonance (EPR) study; and nitric oxide synthases, copper zinc (CuZn) SODs and manganese (Mn) SODs were examined immunohistochemically, (3) and (4) I/R injury was assessed in rats that had received intraperitoneal injections of L-arginine (NO donor) and L-NAME (NO antagonist), respectively. Results: For premature (1,2), newborn (3) and mature (4,5) intestines, grades of injury at maximum I/R period studied (120 minutes of ischemia, 25 minutes of reperfusion) were 0, 0, and 3, respectively (P < .05); NO levels were 1 u ± 1.5, 3 ± 2.5, and 22 u ± 3.5, respectively (P < .05); Cu levels were 150 u ± 15, 200 u ± 41 and 12 u ± 2, respectively (P < .05); NOS in intestines were +, +, +++ and CuZnSODs were ++, +++, +, respectively; and MnSODs were +++, ++, -, respectively. No change in NO levels was detected in groups (1), (2), or (3) after L-arginine and L-NAME injections. Conclusions: Premature rat intestine is highly resistant to I/R injury, which may indicate that I/R alone, in the absence of other predisposing factors (eg, bacterial colonization) may not be sufficient in causing NEC. Nitric oxide does not have a protective role for immature and newborn intestines in I/R as in mature intestine. The high level of SODs of the immature and newborn intestine may play an important role in its high resistance to I/R injury. Copyright 2002, Elsevier Science (USA). All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67386
ISSN
2015 Impact Factor: 1.733
2015 SCImago Journal Rankings: 0.802
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, KLen_HK
dc.contributor.authorHui, CWCen_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorFung, PCWen_HK
dc.contributor.authorWo, JYHen_HK
dc.contributor.authorTipoe, Gen_HK
dc.contributor.authorTam, PKHen_HK
dc.date.accessioned2010-09-06T05:54:41Z-
dc.date.available2010-09-06T05:54:41Z-
dc.date.issued2002en_HK
dc.identifier.citationJournal Of Pediatric Surgery, 2002, v. 37 n. 6, p. 828-834en_HK
dc.identifier.issn0022-3468en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67386-
dc.description.abstractBackground/Purpose: The pathogenesis of necrotizing enterocolitis (NEC) is unknown. Ischemia and reperfusion (I/R) injury has been considered a major contributing factor. Nitric oxide (NO) and superoxide dismutases (SODs) have been shown to protect bowel from I/R injury. This study aims to assess (1) the ability of premature intestine to resist I/R injury compared with mature intestine and (2) the possible role of NO and SODs in modulating such response. Methods: Intestines from 5 groups of rats (n = 6 for each study group) were studied: (1) premature, gestational age 20 days; (2) premature, gestational age 22 days; (3) full-term, newborn; (4) infant, day 15; (5) infant, day 30. Experiments: (1) The degrees of I/R injury after 0, 30, 60, 90 and 120 minutes, respectively, of ischemia and 25 minutes of I/R were assessed histologically by a pathologist who was unaware of the operative details. (2) Tissue NO and copper levels were measured by electroparamagnetic resonance (EPR) study; and nitric oxide synthases, copper zinc (CuZn) SODs and manganese (Mn) SODs were examined immunohistochemically, (3) and (4) I/R injury was assessed in rats that had received intraperitoneal injections of L-arginine (NO donor) and L-NAME (NO antagonist), respectively. Results: For premature (1,2), newborn (3) and mature (4,5) intestines, grades of injury at maximum I/R period studied (120 minutes of ischemia, 25 minutes of reperfusion) were 0, 0, and 3, respectively (P < .05); NO levels were 1 u ± 1.5, 3 ± 2.5, and 22 u ± 3.5, respectively (P < .05); Cu levels were 150 u ± 15, 200 u ± 41 and 12 u ± 2, respectively (P < .05); NOS in intestines were +, +, +++ and CuZnSODs were ++, +++, +, respectively; and MnSODs were +++, ++, -, respectively. No change in NO levels was detected in groups (1), (2), or (3) after L-arginine and L-NAME injections. Conclusions: Premature rat intestine is highly resistant to I/R injury, which may indicate that I/R alone, in the absence of other predisposing factors (eg, bacterial colonization) may not be sufficient in causing NEC. Nitric oxide does not have a protective role for immature and newborn intestines in I/R as in mature intestine. The high level of SODs of the immature and newborn intestine may play an important role in its high resistance to I/R injury. Copyright 2002, Elsevier Science (USA). All rights reserved.en_HK
dc.languageengen_HK
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/jpedsurgen_HK
dc.relation.ispartofJournal of Pediatric Surgeryen_HK
dc.subjectIschemiaen_HK
dc.subjectNecrotizing enterocolitisen_HK
dc.subjectReperfusion injuryen_HK
dc.titleRevisiting ischemia and reperfusion injury as a possible cause of necrotizing enterocolitis: Role of nitric oxide and superoxide dismutaseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-3468&volume=37&spage=828&epage=834&date=2002&atitle=Revisiting+ischemia+and+reperfusion+injury+as+a+possible+cause+of+necrotizing+enterocolitis:+role+of+nitric+oxide+and+superoxide+dismutaseen_HK
dc.identifier.emailChan, KW:hrmtckw@hku.hken_HK
dc.identifier.emailTipoe, G:tgeorge@hkucc.hku.hken_HK
dc.identifier.emailTam, PKH:paultam@hkucc.hku.hken_HK
dc.identifier.authorityChan, KW=rp00330en_HK
dc.identifier.authorityTipoe, G=rp00371en_HK
dc.identifier.authorityTam, PKH=rp00060en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1053/jpsu.2002.32882en_HK
dc.identifier.pmid12037744-
dc.identifier.scopuseid_2-s2.0-0035987643en_HK
dc.identifier.hkuros69024en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035987643&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume37en_HK
dc.identifier.issue6en_HK
dc.identifier.spage828en_HK
dc.identifier.epage834en_HK
dc.identifier.isiWOS:000175982100004-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChan, KL=37004089600en_HK
dc.identifier.scopusauthoridHui, CWC=8204532800en_HK
dc.identifier.scopusauthoridChan, KW=16444133100en_HK
dc.identifier.scopusauthoridFung, PCW=7101613315en_HK
dc.identifier.scopusauthoridWo, JYH=36852841300en_HK
dc.identifier.scopusauthoridTipoe, G=7003550610en_HK
dc.identifier.scopusauthoridTam, PKH=7202539421en_HK

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