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Arginine metabolism in a small animal model of sepsis and after hemihepatectomy
Critical Care volume 13, Article number: P133 (2009)
Introduction
Asymmetric dimethylarginine (ADMA) is an inhibitor of the arginine–NO pathway. ADMA accumulates when degradation in the liver by dimethylarginine dimethylaminohydrolase is impaired. In theory, plasma citrulline, formed when arginine is converted by NO synthase, and when ADMA is metabolized, would be lowered and ornithine, formed by the degradation of arginine in the urea cycle, would be potentially elevated when ADMA accumulates as in sepsis and in liver failure [1].
Methods
Fourteen male Wistar rats were randomly allocated to lipopolysaccharide (LPS) or hemihepatectomy (HH). Plasma levels of arginine, ADMA, citrulline and ornithine were measured before and 120 minutes after 5 mg/kg LPS and HH, respectively.
Results
See Table 1.
Conclusion
Plasma levels of arginine and derivatives should not be interpreted as a reflection of metabolism at the tissue level. In HH, the elevated ADMA levels suggest dimethylarginine dimethylaminohydrolase activity depends on the liver tissue mass.
References
Wu G, et al.: Arginine metabolism: nitric oxide and beyond. Biochem J 1998, 336: 1-17.
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Hoven, B.V.d., Teerlink, T., De Jong, S. et al. Arginine metabolism in a small animal model of sepsis and after hemihepatectomy. Crit Care 13 (Suppl 1), P133 (2009). https://doi.org/10.1186/cc7297
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DOI: https://doi.org/10.1186/cc7297