Pathophysiological and neurochemical mechanisms of postoperative nausea and vomiting.

Autor: Horn CC; Biobehavioral Medicine in Oncology Program, University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA; Department of Medicine, Division of Gastroenterology, Hepatology, and Nutrition, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Department of Anesthesiology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA. Electronic address: chorn@pitt.edu., Wallisch WJ; Department of Anesthesiology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA., Homanics GE; Department of Anesthesiology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, PA, USA; Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA., Williams JP; Department of Anesthesiology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Jazyk: angličtina
Zdroj: European journal of pharmacology [Eur J Pharmacol] 2014 Jan 05; Vol. 722, pp. 55-66. Date of Electronic Publication: 2013 Oct 26.
DOI: 10.1016/j.ejphar.2013.10.037
Abstrakt: Clinical research shows that postoperative nausea and vomiting (PONV) is caused primarily by the use of inhalational anesthesia and opioid analgesics. PONV is also increased by several risk predictors, including a young age, female sex, lack of smoking, and a history of motion sickness. Genetic studies are beginning to shed light on the variability in patient experiences of PONV by assessing polymorphisms of gene targets known to play roles in emesis (serotonin type 3, 5-HT3; opioid; muscarinic; and dopamine type 2, D2, receptors) and the metabolism of antiemetic drugs (e.g., ondansetron). Significant numbers of clinical trials have produced valuable information on pharmacological targets important for controlling PONV (e.g., 5-HT3 and D2), leading to the current multi-modal approach to inhibit multiple sites in this complex neural system. Despite these significant advances, there is still a lack of fundamental knowledge of the mechanisms that drive the hindbrain central pattern generator (emesis) and forebrain pathways (nausea) that produce PONV, particularly the responses to inhalational anesthesia. This gap in knowledge has limited the development of novel effective therapies of PONV. The current review presents the state of knowledge on the biological mechanisms responsible for PONV, summarizing both preclinical and clinical evidence. Finally, potential ways to advance the research of PONV and more recent developments on the study of postdischarge nausea and vomiting (PDNV) are discussed.
(© 2013 Published by Elsevier B.V.)
Databáze: MEDLINE
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