File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Graft Injury in Relation to Graft Size in Right Lobe Live Donor Liver Transplantation: A Study of Hepatic Sinusoidal Injury in Correlation with Portal Hemodynamics and Intragraft Gene Expression

TitleGraft Injury in Relation to Graft Size in Right Lobe Live Donor Liver Transplantation: A Study of Hepatic Sinusoidal Injury in Correlation with Portal Hemodynamics and Intragraft Gene Expression
Authors
Issue Date2003
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.annalsofsurgery.com
Citation
Annals Of Surgery, 2003, v. 237 n. 2, p. 256-264 How to Cite?
AbstractObjective: To investigate the degree and mechanism of hepatic sinusoidal injury in different graft sizes in right lobe live donor liver transplantation (LDLT). Summary Background Data: Liver grafts from living donors are likely to be small-for-size for adult recipients. Graft injury after reperfusion is common, but the mechanism and degree of injury remain unclear. The hepatic sinusoidal injury in different graft sizes and its relationship with portal hemodynamics and intragraft gene response at the early phase after reperfusion have not been studied in right lobe LDLT. Methods: From May 2000 to November 2001, 40 adults receiving right lobe LDLT had portal pressure measured continuously before and after reperfusion. Liver biopsies were taken before and after reperfusion for detection of vasoregulatory genes (endothelin-1 and endothelial nitric oxide synthase) and heat shock genes (heat shock protein 70 and heme oxygenase-1), and electron microscope examination. Blood samples from the portal vein and suprahepatic inferior vena cava were taken for the measurement of plasma nitric oxide level. Results: The recipients were grouped according to the ratio of graft weight to estimated standard liver weight: group 1 (n = 10), less than 40%; group 2 (n = 21), 40% to 60%; and group 3 (n = 9), more than 60%. The portal pressures recorded after reperfusion in group 1 were significantly higher within 30 minutes of reperfusion than those in groups 2 and 3. After reperfusion, the intragraft endothelin-1 mRNA level in group 1 increased by 161% of the basal level but decreased by 31.5% and 62% of the basal level in groups 2 and 3, respectively. The intragraft mRNA level of heme oxygenase-1 in groups 1 and 2 decreased by 75.5% and 25.3% of the basal level respectively but increased by 41% of basal level in group 3. The intragraft protein level of heat shock protein 70 decreased by 50 ng/mL after reperfusion in group 1 but increased by 12.4 ng/mL and 0.6 ng/mL in groups 2 and 3, respectively. The portal vein plasma nitric oxide level decreased more significantly after reperfusion in group 1 than in group 2. Electron microscope examination of liver biopsies in group 1 showed tremendous mitochondrial swelling as well as irregular large gaps between the sinusoidal lining cells. There were two hospital deaths in group 1 and none in the other two groups. Conclusions: Patients implanted with grafts less than 40% of standard liver weight suffered from transient portal hypertension early after reperfusion. The phenomenon was accompanied by intragraft upregulation of endothelin-1 and ultrastructural evidence of sinusoidal damage. The transient portal hypertension after reperfusion, subsequent endothelin-1 overexpression, and plasma nitric oxide level reduction, together with downregulation of heme oxygenase-1 and heat shock protein 70, may account for the small-for-size graft injury.
Persistent Identifierhttp://hdl.handle.net/10722/49120
ISSN
2015 Impact Factor: 8.569
2015 SCImago Journal Rankings: 4.503
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMan, Ken_HK
dc.contributor.authorFan, STen_HK
dc.contributor.authorLo, CMen_HK
dc.contributor.authorLiu, CLen_HK
dc.contributor.authorFung, PCWen_HK
dc.contributor.authorLiang, TBen_HK
dc.contributor.authorLee, TKHen_HK
dc.contributor.authorTsui, SHTen_HK
dc.contributor.authorNg, IOLen_HK
dc.contributor.authorZhang, ZWen_HK
dc.contributor.authorWong, Jen_HK
dc.date.accessioned2008-06-12T06:34:52Z-
dc.date.available2008-06-12T06:34:52Z-
dc.date.issued2003en_HK
dc.identifier.citationAnnals Of Surgery, 2003, v. 237 n. 2, p. 256-264en_HK
dc.identifier.issn0003-4932en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49120-
dc.description.abstractObjective: To investigate the degree and mechanism of hepatic sinusoidal injury in different graft sizes in right lobe live donor liver transplantation (LDLT). Summary Background Data: Liver grafts from living donors are likely to be small-for-size for adult recipients. Graft injury after reperfusion is common, but the mechanism and degree of injury remain unclear. The hepatic sinusoidal injury in different graft sizes and its relationship with portal hemodynamics and intragraft gene response at the early phase after reperfusion have not been studied in right lobe LDLT. Methods: From May 2000 to November 2001, 40 adults receiving right lobe LDLT had portal pressure measured continuously before and after reperfusion. Liver biopsies were taken before and after reperfusion for detection of vasoregulatory genes (endothelin-1 and endothelial nitric oxide synthase) and heat shock genes (heat shock protein 70 and heme oxygenase-1), and electron microscope examination. Blood samples from the portal vein and suprahepatic inferior vena cava were taken for the measurement of plasma nitric oxide level. Results: The recipients were grouped according to the ratio of graft weight to estimated standard liver weight: group 1 (n = 10), less than 40%; group 2 (n = 21), 40% to 60%; and group 3 (n = 9), more than 60%. The portal pressures recorded after reperfusion in group 1 were significantly higher within 30 minutes of reperfusion than those in groups 2 and 3. After reperfusion, the intragraft endothelin-1 mRNA level in group 1 increased by 161% of the basal level but decreased by 31.5% and 62% of the basal level in groups 2 and 3, respectively. The intragraft mRNA level of heme oxygenase-1 in groups 1 and 2 decreased by 75.5% and 25.3% of the basal level respectively but increased by 41% of basal level in group 3. The intragraft protein level of heat shock protein 70 decreased by 50 ng/mL after reperfusion in group 1 but increased by 12.4 ng/mL and 0.6 ng/mL in groups 2 and 3, respectively. The portal vein plasma nitric oxide level decreased more significantly after reperfusion in group 1 than in group 2. Electron microscope examination of liver biopsies in group 1 showed tremendous mitochondrial swelling as well as irregular large gaps between the sinusoidal lining cells. There were two hospital deaths in group 1 and none in the other two groups. Conclusions: Patients implanted with grafts less than 40% of standard liver weight suffered from transient portal hypertension early after reperfusion. The phenomenon was accompanied by intragraft upregulation of endothelin-1 and ultrastructural evidence of sinusoidal damage. The transient portal hypertension after reperfusion, subsequent endothelin-1 overexpression, and plasma nitric oxide level reduction, together with downregulation of heme oxygenase-1 and heat shock protein 70, may account for the small-for-size graft injury.en_HK
dc.format.extent388 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.annalsofsurgery.comen_HK
dc.relation.ispartofAnnals of Surgeryen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshGene Expression Regulation - physiologyen_HK
dc.subject.meshHypertension, Portal - etiology - physiopathologyen_HK
dc.subject.meshLiver Transplantation - adverse effects - pathology - physiologyen_HK
dc.subject.meshLiver Circulation - physiologyen_HK
dc.subject.meshLiving Donorsen_HK
dc.titleGraft Injury in Relation to Graft Size in Right Lobe Live Donor Liver Transplantation: A Study of Hepatic Sinusoidal Injury in Correlation with Portal Hemodynamics and Intragraft Gene Expressionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0003-4932&volume=237&issue=2&spage=256&epage=264&date=2003&atitle=Graft+injury+in+relation+to+graft+size+in+right+lobe+live+donor+liver+transplantation:+a+study+of+hepatic+sinusoidal+injury+in+correlation+with+portal+hemodynamics+and+intragraft+gene+expressionen_HK
dc.identifier.emailMan, K: kwanman@hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hken_HK
dc.identifier.emailLee, TKH: tkwlee@hkucc.hku.hken_HK
dc.identifier.emailNg, IOL: iolng@hku.hken_HK
dc.identifier.emailWong, J: jwong@hkucc.hku.hken_HK
dc.identifier.authorityMan, K=rp00417en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.identifier.authorityLo, CM=rp00412en_HK
dc.identifier.authorityLee, TKH=rp00447en_HK
dc.identifier.authorityNg, IOL=rp00335en_HK
dc.identifier.authorityWong, J=rp00322en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1097/00000658-200302000-00015en_HK
dc.identifier.pmid12560784-
dc.identifier.pmcidPMC1522144en_HK
dc.identifier.scopuseid_2-s2.0-0037316049en_HK
dc.identifier.hkuros76918-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037316049&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume237en_HK
dc.identifier.issue2en_HK
dc.identifier.spage256en_HK
dc.identifier.epage264en_HK
dc.identifier.isiWOS:000185833900015-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridMan, K=7101754072en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK
dc.identifier.scopusauthoridLo, CM=7401771672en_HK
dc.identifier.scopusauthoridLiu, CL=7409789712en_HK
dc.identifier.scopusauthoridFung, PCW=7101613315en_HK
dc.identifier.scopusauthoridLiang, TB=7202019213en_HK
dc.identifier.scopusauthoridLee, TKH=7501439435en_HK
dc.identifier.scopusauthoridTsui, SHT=7004961357en_HK
dc.identifier.scopusauthoridNg, IOL=7102753722en_HK
dc.identifier.scopusauthoridZhang, ZW=8574700400en_HK
dc.identifier.scopusauthoridWong, J=8049324500en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats