RGD Reference Report - Topical hepatic hypothermia attenuates pulmonary injury after hepatic ischemia and reperfusion. - Rat Genome Database

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Topical hepatic hypothermia attenuates pulmonary injury after hepatic ischemia and reperfusion.

Authors: Patel, S  Pachter, H L  Yee, H  Schwartz, J D  Marcus, S G  Shamamian, P 
Citation: Patel S, etal., J Am Coll Surg. 2000 Dec;191(6):650-6. doi: 10.1016/s1072-7515(00)00736-5.
RGD ID: 14995473
Pubmed: PMID:11129814   (View Abstract at PubMed)
DOI: DOI:10.1016/s1072-7515(00)00736-5   (Journal Full-text)


BACKGROUND: Prolonged periods of hepatic ischemia are associated with hepatocellular injury and distant organ dysfunction in experimental models. Neutrophils (PMN) and tumor necrosis factor (TNF)-alpha have been implicated, mostly because of their local deleterious effects on the hepatocyte after hepatic ischemia and reperfusion (I/R) injury. We hypothesize that topical hepatic hypothermia (THH) reduces ischemia and reperfusion-induced hepatic necrosis, PMN infiltration, TNF-alpha release, and consequent acute pulmonary injury.
STUDY DESIGN: Sprague-Dawley rats (250 to 300g) were evenly divided into three groups: 90 minutes of normothermic (37 degrees C) partial hepatic ischemia (normothermic I/R), 90 minutes of hypothermic (25 degrees C) partial hepatic ischemia (hypothermic I/R), and sham laparotomy (without ischemia). There were six animals in each experimental group per time point unless otherwise specified. Hepatic necrosis and PMN infiltration were evaluated and scored on hematoxylin and eosin-stained liver specimens 12 hours after reperfusion. Serum TNF-alpha levels were determined by ELISA at 0 minutes, 15 minutes, 30 minutes, 1 hour, and 12 hours postreperfusion. Pulmonary PMN infiltration and vascular permeability were measured by myeloperoxidase activity and Evans blue dye extravasation, respectively, to quantitate pulmonary injury 12 hours after reperfusion.
RESULTS: Normothermic I/R results in a significant increase in TNF-alpha at 15 and 30 minutes (p < 0.005), PMN infiltration (p < 0.001), and hepatic necrosis (p < 0.001), compared with sham. Institution of THH reduced peak serum TNF-alpha levels by 54% at 15 minutes (p < 0.005) and by 73% at 30 minutes (p < 0.001) postreperfusion compared with normothermic I/R. Similarly, hepatic PMN infiltration and necrosis at 12 hours were reduced by 60% (p < 0.05) and 47% (p < 0.05), respectively. Myeloperoxidase activity and Evans blue extravasation (measures of acute lung injury) were reduced by 42% and 39%, respectively, with institution of THH compared with animals undergoing normothermic I/R (p < 0.001).
CONCLUSIONS: These results demonstrate that THH protects the liver from ischemia and reperfusion-induced necrosis and PMN infiltration. In addition, THH reduces the serum levels of TNF-alpha and associated pulmonary injury. These data suggest that the ischemic liver is a potential source of inflammatory mediators associated with hepatic ischemia and reperfusion-induced pulmonary injury.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
TNFHumanAcute Lung Injury treatmentISOTnf (Rattus norvegicus)associated with Liver Reperfusion InjuryRGD 
TnfRatAcute Lung Injury treatmentIEP associated with Liver Reperfusion InjuryRGD 
TnfMouseAcute Lung Injury treatmentISOTnf (Rattus norvegicus)associated with Liver Reperfusion InjuryRGD 
TNFHumanLiver Reperfusion Injury treatmentISOTnf (Rattus norvegicus) RGD 
TnfRatLiver Reperfusion Injury treatmentIEP  RGD 
TnfMouseLiver Reperfusion Injury treatmentISOTnf (Rattus norvegicus) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Tnf  (tumor necrosis factor)

Genes (Mus musculus)
Tnf  (tumor necrosis factor)

Genes (Homo sapiens)
TNF  (tumor necrosis factor)


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