Moderate hypercapnia exerts beneficial effects on splanchnic energy metabolism during endotoxemia.
Détails
Etat: Public
Version: Final published version
Licence: Non spécifiée
It was possible to publish this article open access thanks to a Swiss National Licence with the publisher.
ID Serval
serval:BIB_FBEEF977BEB8
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Moderate hypercapnia exerts beneficial effects on splanchnic energy metabolism during endotoxemia.
Périodique
Intensive care medicine
ISSN
1432-1238[electronic]
Statut éditorial
Publié
Date de publication
2009
Volume
35
Numéro
7
Pages
1297-1304
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Publication Status: ppublish
Résumé
PURPOSE: Low tidal volume ventilation and permissive hypercapnia are required in patients with sepsis complicated by ARDS. The effects of hypercapnia on tissue oxidative metabolism in this setting are unknown. We therefore determined the effects of moderate hypercapnia on markers of systemic and splanchnic oxidative metabolism in an animal model of endotoxemia. METHODS: Anesthetized rats maintained at a PaCO(2) of 30, 40 or 60 mmHg were challenged with endotoxin. A control group (PaCO(2) 40 mmHg) received isotonic saline. Hemodynamic variables, arterial lactate, pyruvate, and ketone bodies were measured at baseline and after 4 h. Tissue adenosine triphosphate (ATP) and lactate were measured in the small intestine and the liver after 4 h. RESULTS: Endotoxin resulted in low cardiac output, increased lactate/pyruvate ratio and decreased ketone body ratio. These changes were not influenced by hypercapnia, but were more severe with hypocapnia. In the liver, ATP decreased and lactate increased independently from PaCO(2) after endotoxin. In contrast, the drop of ATP and the rise in lactate triggered by endotoxin in the intestine were prevented by hypercapnia. CONCLUSIONS: During endotoxemia in rats, moderate hypercapnia prevents the deterioration of tissue energetics in the intestine.
Mots-clé
Animals, Carbon Dioxide/administration & dosage, Carbon Dioxide/physiology, Endotoxemia/physiopathology, Energy Metabolism/drug effects, Energy Metabolism/physiology, Hypercapnia/metabolism, Oxygen Consumption, Random Allocation, Rats, Rats, Wistar, Respiration, Artificial, Respiratory Distress Syndrome, Adult/physiopathology, Respiratory Distress Syndrome, Adult/therapy, Sepsis/physiopathology, Splanchnic Circulation/drug effects, Splanchnic Circulation/physiology
Pubmed
Web of science
Open Access
Oui
Création de la notice
21/12/2009 13:36
Dernière modification de la notice
14/02/2022 8:57