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Sustained elevation of norepinephrine depresses hepatocellular function
P Wang1, S M Tait, I H Chaudry
1Department of Surgery, University of Alabama at Birmingham School of Medicine, 1670 University Boulevard, Volker Hall, Room G094P, Birmingham, AL 35294-0019, USA. ping.wang@ccc.uab.edu
Biochimica Et Biophysica Acta
|December 13, 2000
Summary
Sustained high levels of norepinephrine (NE) significantly impair liver function and cause injury, even without sepsis or shock. This study demonstrates NE
Area of Science:
- Physiology
- Hepatology
- Pharmacology
Background:
- Sepsis and hemorrhagic shock activate the sympathetic-adrenal system, increasing catecholamines.
- Hepatocellular dysfunction during shock correlates with elevated plasma norepinephrine (NE).
- The direct role of NE in causing hepatocellular dysfunction remains unclear.
Purpose of the Study:
- To investigate if elevated norepinephrine (NE) alone causes hepatocellular dysfunction.
- To determine the effects of sustained NE increase on cardiac output, organ perfusion, and liver function.
Main Methods:
- Exogenous NE was administered via osmotic pumps to mimic shock-related NE levels.
- Cardiac output, hepatocellular function (indocyanine green clearance Vmax and Km), and organ perfusion were assessed.
- Interleukin-6 and liver enzymes were measured.
Main Results:
- Sustained NE elevation decreased cardiac output and microvascular blood flow in the liver, spleen, and intestines.
- Hepatocellular function (Vmax and Km) was significantly depressed by elevated NE.
- Increased NE led to elevated liver enzymes and interleukin-6, indicating liver injury.
Conclusions:
- Sustained high plasma norepinephrine levels can directly cause hepatocellular dysfunction.
- Elevated NE contributes to liver injury and altered hepatocyte integrity.
- These findings highlight NE's critical role in shock-induced liver damage.