Hepatocellular Transplantation for Metabolic Support in Experimental Acute Ischemic Liver Failure in Rats

The function of transplanted hepatocytes in acute ischemic liver failure was studied in an experimental model using rats. Ischemic liver failure was induced by occlusion of the proximal portal vein and hepatic artery immediately following extracorporeal portofemoral venous bypass. All rats were bred...

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Main Authors: Kazuyoshi Takeshita, Haruaki Ishibashi, Masayuki Suzuki, Masashi Kodama
Format: Article
Language:English
Published: SAGE Publishing 1993-07-01
Series:Cell Transplantation
Online Access:https://doi.org/10.1177/096368979300200414
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spelling doaj-9d649a02f40849e19828bdc6e3f3ad9c2020-11-25T01:20:38ZengSAGE PublishingCell Transplantation0963-68971555-38921993-07-01210.1177/096368979300200414Hepatocellular Transplantation for Metabolic Support in Experimental Acute Ischemic Liver Failure in RatsKazuyoshi Takeshita0Haruaki Ishibashi1Masayuki Suzuki2Masashi Kodama3First Department of Surgery, Shiga University of Medical ScienceFirst Department of Surgery, Shiga University of Medical ScienceFirst Department of Surgery, Shiga University of Medical ScienceFirst Department of Surgery, Shiga University of Medical ScienceThe function of transplanted hepatocytes in acute ischemic liver failure was studied in an experimental model using rats. Ischemic liver failure was induced by occlusion of the proximal portal vein and hepatic artery immediately following extracorporeal portofemoral venous bypass. All rats were bred in a closed colony. Rats in Group 1 were untreated and served as controls (n = 10). Rats in Group 2 received an intrasplenic transplant of hepatocytes (1 × 107 cells) 48 h before liver ischemia (n = 10). Serum ammonia and blood glucose were measured before, and 1 h after, ischemia. Serum ammonia was significantly higher than normal (Group 1, 930 μg/dL vs < 110 μg/dL) after liver ischemia. On the other hand, serum ammonia in group 2 also was elevated (355 μg/dL), but significantly less so than in Group 1 (p < 0.001). Blood glucose was lower in both groups after liver ischemia, compared to normal (50-100 mg/dL), but it was higher in Group 2 (30 mg/dL) than in Group 1 (14 mg/dL, p < 0.01). Liver histology 1 h after ischemia showed similar degrees of necrosis in the two groups. Transplanted hepatocytes were viable, and clearly identified in the splenic parenchyma after ischemia. Intrasplenic transplanted hepatocytes provide temporary metabolic support of acute ischemic liver failure in rats, as reflected by enhanced ammonia removal and gluconeogenesis.https://doi.org/10.1177/096368979300200414
collection DOAJ
language English
format Article
sources DOAJ
author Kazuyoshi Takeshita
Haruaki Ishibashi
Masayuki Suzuki
Masashi Kodama
spellingShingle Kazuyoshi Takeshita
Haruaki Ishibashi
Masayuki Suzuki
Masashi Kodama
Hepatocellular Transplantation for Metabolic Support in Experimental Acute Ischemic Liver Failure in Rats
Cell Transplantation
author_facet Kazuyoshi Takeshita
Haruaki Ishibashi
Masayuki Suzuki
Masashi Kodama
author_sort Kazuyoshi Takeshita
title Hepatocellular Transplantation for Metabolic Support in Experimental Acute Ischemic Liver Failure in Rats
title_short Hepatocellular Transplantation for Metabolic Support in Experimental Acute Ischemic Liver Failure in Rats
title_full Hepatocellular Transplantation for Metabolic Support in Experimental Acute Ischemic Liver Failure in Rats
title_fullStr Hepatocellular Transplantation for Metabolic Support in Experimental Acute Ischemic Liver Failure in Rats
title_full_unstemmed Hepatocellular Transplantation for Metabolic Support in Experimental Acute Ischemic Liver Failure in Rats
title_sort hepatocellular transplantation for metabolic support in experimental acute ischemic liver failure in rats
publisher SAGE Publishing
series Cell Transplantation
issn 0963-6897
1555-3892
publishDate 1993-07-01
description The function of transplanted hepatocytes in acute ischemic liver failure was studied in an experimental model using rats. Ischemic liver failure was induced by occlusion of the proximal portal vein and hepatic artery immediately following extracorporeal portofemoral venous bypass. All rats were bred in a closed colony. Rats in Group 1 were untreated and served as controls (n = 10). Rats in Group 2 received an intrasplenic transplant of hepatocytes (1 × 107 cells) 48 h before liver ischemia (n = 10). Serum ammonia and blood glucose were measured before, and 1 h after, ischemia. Serum ammonia was significantly higher than normal (Group 1, 930 μg/dL vs < 110 μg/dL) after liver ischemia. On the other hand, serum ammonia in group 2 also was elevated (355 μg/dL), but significantly less so than in Group 1 (p < 0.001). Blood glucose was lower in both groups after liver ischemia, compared to normal (50-100 mg/dL), but it was higher in Group 2 (30 mg/dL) than in Group 1 (14 mg/dL, p < 0.01). Liver histology 1 h after ischemia showed similar degrees of necrosis in the two groups. Transplanted hepatocytes were viable, and clearly identified in the splenic parenchyma after ischemia. Intrasplenic transplanted hepatocytes provide temporary metabolic support of acute ischemic liver failure in rats, as reflected by enhanced ammonia removal and gluconeogenesis.
url https://doi.org/10.1177/096368979300200414
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AT masayukisuzuki hepatocellulartransplantationformetabolicsupportinexperimentalacuteischemicliverfailureinrats
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