Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2847273 | Respiratory Physiology & Neurobiology | 2013 | 6 Pages |
Copeptin, the C-terminal part of the arginine vasopressin precursor peptide, holds promise as a diagnostic and prognostic plasma biomarker in various acute clinical conditions. Factors influencing copeptin response in the critical care setting are only partially established and have not been investigated systematically. Using an in vivo infant ventilation model (Wistar rats, 14 days old), we studied the influence of commonly occurring stressors in critically ill children. In unstressed ventilated rats basal median copeptin concentration was 22 pmol/L. In response to respiratory alkalosis copeptin increased 5-fold, while exposure to hypoxemia, high PEEP, hemorrhage, and psycho-emotional stress produced a more than 10-fold increase. Additionally, we did not find a direct association between copeptin and acidosis, hypercapnia, and hyperthermia. Clinicians working in the acute critical care setting should be aware of factors influencing copeptin plasma concentrations. Moreover, our results do have implications for animal studies in the field of stress research.
► Copeptin is a sensitive and early responsive biomarker in critical care diseases. ► Alkalosis, hypoxemia, hemorrhage, and PEEP produce significant copeptin responses. ► Acidosis, body temperature, and protective ventilation do not influence copeptin. ► Apparently unstressed non-ventilated animals showed clearly increased copeptin values. ► Copeptin concentration can also be measured quantitatively in an in vivo animal model.