Bile secretory function after warm hepatic ischemia-reperfusion injury in the rat

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dc.contributor.authorAccatino, L
dc.contributor.authorPizarro, M
dc.contributor.authorSolis, N
dc.contributor.authorArrese, M
dc.contributor.authorKoenig, CS
dc.date.accessioned2024-01-10T12:37:48Z
dc.date.available2024-01-10T12:37:48Z
dc.date.issued2003
dc.description.abstractHepatic ischemia-reperfusion (I-R) injury frequently is associated with cholestasis. However, the underlying mechanisms are not fully understood. The aim of the study is to assess bile secretory function in vivo in rats subjected to warm lobar hepatic ischemia at different times during reperfusion. A model of lobar 70% warm hepatic ischemia for 30 minutes was used with studies conducted at 1 and 6 hours and 1, 3, and 7 days after reperfusion. Bile secretory function was assessed after selective cannulation of bile ducts of ischemic (ILs) and nonischemic lobes (NILs). Serum activity of hepatic alanine and aspartate aminotransferase was slightly increased in rats subjected to I-R, whereas serum bile salt levels increased early during reperfusion, returning to control values after 7 days. ILs; showed mild reversible leukocyte infiltration and no significant necrosis. Bile flow and bile salt excretion were significantly decreased in ILs during the first 24-hour reperfusion period compared with shamoperated rats and NILs. A marked reduction in glutathione (GSH) excretion occurred at I and 6 hours and I and 3 days, which returned to control values after 7 days. Total GSH and both reduced and oxidized GSH levels in liver homogenate and arterial blood GSH levels were unchanged at all times. Protein mass of multidrug resistance protein 2 and its function, assessed by the hepatic maximum secretory rate of ceftriaxone, did not show significant changes in ILs or NILs compared with shamoperated rats. Liver tissue gamma-glutamyl transpeptidase (GGT) and gamma-glutamylcysteine synthetase activities remained unchanged, whereas biliary GGT and cysteine secretory rates were significantly increased in ILs; and NILs. Administration of acivicin, a GGT inhibitor, resulted in decreased secretion of this enzyme into bile and a parallel marked increase in biliary GSH secretion compared with untreated ischemic rats. In conclusion, warm hepatic I-R induces reversible cholestatic changes in ILs. GSH secretory rates from both ILs and NILs were markedly decreased during reperfusion. The reversibility of this effect after GGT inhibition, as well as increased release of active GGT into bile and cysteine biliary secretory rates, suggest increased GSH degradation in bile. These findings might be relevant for the I-R-induced clinical cholestasis, as well as cholangiocyte injury, seen after hepatic ischemia.
dc.fechaingreso.objetodigital2024-04-25
dc.format.extent12 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1053/jlts.2003.50232
dc.identifier.eissn1527-6473
dc.identifier.issn1527-6465
dc.identifier.pubmedidMEDLINE:14586882
dc.identifier.urihttps://doi.org/10.1053/jlts.2003.50232
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/76926
dc.identifier.wosidWOS:000186270400011
dc.information.autorucMedicina;Accatino L;S/I;99016
dc.information.autorucMedicina;Arrese M;S/I;76095
dc.issue.numero11
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final1210
dc.pagina.inicio1199
dc.publisherWILEY
dc.revistaLIVER TRANSPLANTATION
dc.rightsacceso restringido
dc.subjectORTHOTOPIC LIVER-TRANSPLANTATION
dc.subjectGAMMA-GLUTAMYL-TRANSPEPTIDASE
dc.subjectLIPID SECRETION
dc.subjectISCHEMIA/REPERFUSION INJURY
dc.subjectOBSTRUCTIVE CHOLESTASIS
dc.subjectBILIARY-EXCRETION
dc.subjectGLUTATHIONE
dc.subjectTRANSPORT
dc.subjectFLOW
dc.subjectINHIBITION
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleBile secretory function after warm hepatic ischemia-reperfusion injury in the rat
dc.typeartículo
dc.volumen9
sipa.codpersvinculados99016
sipa.codpersvinculados76095
sipa.indexWOS
sipa.trazabilidadCarga SIPA;09-01-2024
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