Abstract:
:We evaluated the concept that the vascular entrance of both bacterial and nonbacterial particulate material could lead to hepatic parenchymal cell injury, either due to postphagocytic Kupffer cell activity or the margination of activated leukocytes in the liver. Injection of denatured, collagen-coated particles as well as heat-killed bacteria were used as particulate challenges. Hepatic parenchymal cell injury in vivo during postoperative sepsis was evaluated by plasma aspartate aminotransferase (AST) and ornithine carbamyl transferase (OCT) enzyme levels over 3-72 h. AST and OCT levels elevated following either laparotomy plus cecal ligation (mild sepsis) or laparotomy plus cecal ligation with puncture (severe sepsis), with the peak level at 24 h. In addition, the direct intravenous injection of either nonbacterial foreign particles or heat-killed Pseudomonas aeruginosa into normal rats also produced a dose-dependent elevation of AST and OCT. The plasma level of either AST or OCT actually increased 350-400% after injection of the non-bacterial particles. A similar dose related elevation in enzymes followed the intravenous injection of heat-killed Pseudomonas. To differentiate the potential contribution of activated hepatic Kupffer cells versus activated marginated neutrophils to the in vivo hepatic injury, we determined the release of the hepatic specific enzyme OCT by cultured hepatic parenchymal cells when they were exposed to isolated Kupffer cells or isolated PMNs that were activated by exposure to dead bacteria. Bacteria alone when added to cultured hepatocytes did not induce significant OCT release. In contrast, activated PMNs but not Kupffer cells induced a significant (p less than 0.05) release of OCT from parenchymal cells into the culture media. Thus, in vivo transient hepatic parenchymal cell injury with post-operative sepsis may be mediated by the margination of activated PMNs in the liver.
journal_name
J Leukoc Bioljournal_title
Journal of leukocyte biologyauthors
Holman JM Jr,Saba TMdoi
10.1002/jlb.43.3.193subject
Has Abstractpub_date
1988-03-01 00:00:00pages
193-203issue
3eissn
0741-5400issn
1938-3673journal_volume
43pub_type
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journal_title:Journal of leukocyte biology
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abstract::Neuronal damage in HIV infection results mainly from chronic activation of brain tissue and involves inflammation, oxidative stress, and glutamate-related neurotoxicity. Glutamate toxicity acts via two distinct pathways: an excitotoxic one, in which glutamate receptors are hyperactivated, and an oxidative one, in whic...
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journal_title:Journal of leukocyte biology
pub_type: 杂志文章
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journal_title:Journal of leukocyte biology
pub_type: 杂志文章
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更新日期:1993-02-01 00:00:00
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journal_title:Journal of leukocyte biology
pub_type: 杂志文章
doi:10.1002/jlb.64.1.85
更新日期:1998-07-01 00:00:00
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journal_title:Journal of leukocyte biology
pub_type: 杂志文章,评审
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journal_title:Journal of leukocyte biology
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pub_type: 评论,社论
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