RGD Reference Report - Human adrenomedullin and its binding protein attenuate organ injury and reduce mortality after hepatic ischemia-reperfusion. - Rat Genome Database

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Human adrenomedullin and its binding protein attenuate organ injury and reduce mortality after hepatic ischemia-reperfusion.

Authors: Yang, J  Wu, R  Qiang, X  Zhou, M  Dong, W  Ji, Y  Marini, CP  Ravikumar, TS  Wang, P 
Citation: Yang J, etal., Ann Surg. 2009 Feb;249(2):310-7. doi: 10.1097/SLA.0b013e3181961d43.
RGD ID: 7364958
Pubmed: PMID:19212187   (View Abstract at PubMed)
PMCID: PMC2799995   (View Article at PubMed Central)
DOI: DOI:10.1097/SLA.0b013e3181961d43   (Journal Full-text)

OBJECTIVE: To determine whether administration of a vasoactive peptide, human adrenomedullin (AM), in combination with its binding protein (ie, AMBP-1), prevents or minimizes hepatic ischemia-reperfusion (I/R) injury. SUMMARY BACKGROUND DATA: Hepatic I/R injury results from tissue hypoxia and subsequent inflammatory responses. Even though numerous pharmacological modalities and substances have been studied to reduce I/R-induced mortality, none have been entirely successful. We have shown that administration of AM/AMBP-1 produces significant beneficial effects under various pathophysiological conditions. However, it remains unknown if human AM/AMBP-1 has any protective effects on hepatic I/R-induced tissue damage and mortality. METHODS: Seventy percent hepatic ischemia was induced in male adult rats by placing a microvascular clip across the hilum of the left and median lobes for 90 minutes. After removing the clip, human AM alone, human AMBP-1 alone, human AM in combination with human AMBP-1 or vehicle was administered intravenously over a period of 30 minutes. Blood and tissue samples were collected 4 hours after reperfusion for various measurements. In additional groups of animals, the nonischemic liver lobes were resected at the end of 90-minute ischemia. The animals were monitored for 7 days and survival was recorded. RESULTS: After hepatic I/R, plasma levels of AM were significantly increased, whereas AMBP-1 levels were markedly decreased. Likewise, gene expression of AM in the liver was increased significantly, whereas AMBP-1 expression was markedly decreased. Administration of AM in combination with AMBP-1 immediately after the onset of reperfusion down-regulated inflammatory cytokines, decreased hepatic neutrophil infiltration, inhibited liver cell apoptosis and necrosis, and reduced liver injury and mortality in a rat model of hepatic I/R. On the other hand, administration of human AM alone or human AMBP-1 alone after hepatic I/R failed to produce significant protection. CONCLUSIONS: Human AM/AMBP-1 may be a novel treatment to attenuate tissue injury after an episode of hepatic ischemia.

RGD Manual Disease Annotations    Click to see Annotation Detail View

Objects Annotated

Genes (Rattus norvegicus)
Adm  (adrenomedullin)
Cfh  (complement factor H)

Genes (Mus musculus)
Adm  (adrenomedullin)
Cfh  (complement component factor h)

Genes (Homo sapiens)
ADM  (adrenomedullin)
CFH  (complement factor H)


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