2009
DOI: 10.1007/s11605-008-0796-0
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Hemorrhage-Induced Hepatic Injury and Hypoperfusion can be Prevented by Direct Peritoneal Resuscitation

Abstract: Background-Crystalloid fluid resuscitation after hemorrhagic shock (HS) that restores/maintains central hemodynamics often culminates in multi-system organ failure and death due to persistent/ progressive splanchnic hypoperfusion and end-organ damage. Adjunctive direct peritoneal resuscitation (DPR) using peritoneal dialysis solution reverses HS-induced splanchnic hypoperfusion and improves survival. We examined HS-mediated hepatic perfusion (galactose clearance), tissue injury (histopathology), and dysfunctio… Show more

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Cited by 26 publications
(18 citation statements)
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“…Once TLR-4s are activated, Kupffer cells produce large amounts of cytokines and chemokines including TNF-␣, INF-␥, IL-6, IL-8, MCP-1, IL-17, and CXCL-10. Our previous data demonstrated elevated liver enzymes following HS, and we found elevated serum HMGB1 in this study (8,21,30). Adjunct DPR prevented hepatocyte cell death (HMB1) and improved liver histopathology scores and serum liver enzymes compared with HSϩCR alone.…”
Section: Discussionsupporting
confidence: 69%
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“…Once TLR-4s are activated, Kupffer cells produce large amounts of cytokines and chemokines including TNF-␣, INF-␥, IL-6, IL-8, MCP-1, IL-17, and CXCL-10. Our previous data demonstrated elevated liver enzymes following HS, and we found elevated serum HMGB1 in this study (8,21,30). Adjunct DPR prevented hepatocyte cell death (HMB1) and improved liver histopathology scores and serum liver enzymes compared with HSϩCR alone.…”
Section: Discussionsupporting
confidence: 69%
“…Patients who developed high serum levels of bilirubin, a serum marker of liver injury, had longer stays in the intensive care unit and higher mortality (16.2% vs. 2.5%) compared with patients with normal or slightly elevated bilirubin. While these observational studies suggest an association between HS and significant liver dysfunction, necrosis, and mortality, the mechanisms of this liver injury have not been well defined.Experimental evidence suggests that despite return of central hemodynamic performance by aggressive intravenous fluid resuscitation, the gut and liver experience a progressive vasoconstriction and hypoperfusion after HS (5,14,21,42). End organ tissue hypoperfusion has been linked to several mechanisms of postresuscitation (post-RES) injury: endothelial cell dysfunction, tissue hypoxia, compromised capillary filling and fluid exchange, deranged electrolyte handling, and altered release of cytokine mediators that exaggerate the systemic inflammatory response (40).…”
mentioning
confidence: 99%
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“…In mehreren Studien sowie im Tiermodell haben sich posttraumatische Leberschäden, insbesondere Schäden an den intrahepatischen Gallenwegen, bei einer schweren Hypotonie mit einem systolischen Blutdruck von <100 mmHg und Hypovolamie eingestellt [6,9,13]. Ursache der Schäden an den intrahepatischen Gallenwegen ist die besondere arterielle Versorgung der Gallengangsepithelzellen.…”
Section: Hypotonie Im Splanchnikusgebietunclassified