 |
|
Plasma  -Glutathione S-Transferase
A Sensitive Indicator of Hepatocellular Damage During Polymicrobial Sepsis
Douglas J. Koo, BA;
Mian Zhou, MD;
Irshad H. Chaudry, PhD;
Ping Wang, MD
Arch Surg. 2000;135:198-203.
Hypothesis Since studies have found the liver enzyme  -glutathione S-transferase (GST) to be a marker of hepatic injury after hemorrhagic shock, GST also may serve as a sensitive indicator of hepatocellular damage during the early stage of polymicrobial sepsis.
Design, Interventions, and Main Outcome Measures Male adult rats were subjected to the cecal ligation and puncture (CLP) model of polymicrobial sepsis or sham operation, followed by fluid resuscitation with isotonic sodium chloride solution. Systemic blood samples were taken at 2, 5, 10, or 20 hours after CLP or sham operation. Plasma levels of GST and lactate were determined using an enzyme immunoassay and enzymatic assay, respectively. Additional animals were examined for morphologic alterations in liver ultrastructure of septic animals using electron microscopy.
Results A similar level of GST (mean ± SEM, 30.5 ± 3.5 µg/L) was found in the sham group at all measured time points. Although plasma levels of GST did not change at 2 hours after CLP, they were elevated by 249% at 5 hours after the onset of sepsis and continued to increase throughout the septic course. Plasma lactate levels were significantly increased only at 20 hours after CLP (P<.001). Previous studies have shown that liver transaminase levels did not increase at 5 hours, but at 10 and 20 hours after CLP. In addition, electron microscopy revealed structural changes in hepatocyte morphology at 5 and 20 hours after CLP that were indicative of hepatocellular injury.
Conclusion Since plasma GST levels increased earlier than plasma lactate and liver transaminase levels, GST may be a more sensitive indicator of early liver injury and should be used in monitoring hepatocellular damage during the progression of sepsis.
From the Center for Surgical Research and Department of Surgery, Brown University School of Medicine and Rhode Island Hospital, Providence.
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
The Effect of Inhibition of a Major Cell Signaling Pathway Following Trauma Hemorrhage on Hepatic Injury and Interleukin 6 Levels
Jarrar et al.
Arch Surg 2004;139:896-901.
ABSTRACT
| FULL TEXT
Norepinephrine-induced hepatocellular dysfunction in early sepsis is mediated by activation of alpha 2-adrenoceptors
Yang et al.
Am. J. Physiol. Gastrointest. Liver Physiol. 2001;281:G1014-G1021.
ABSTRACT
| FULL TEXT
Gut-derived norepinephrine plays a critical role in producing hepatocellular dysfunction during early sepsis
Yang et al.
Am. J. Physiol. Gastrointest. Liver Physiol. 2000;279:G1274-G1281.
ABSTRACT
| FULL TEXT
|
