Alveolar but not intravenous S-ketamine inhibits alveolar sodium transport and lung fluid clearance in rats

Autor: Catharina W. Wieland, Stefanie Zügel, Bernhard Pitzer, Marc M. Berger, Albert Dahan, Heimo Mairbäurl, Markus W. Hollmann, Peter Bärtsch, Marcus J. Schultz, Alexander P.J. Vlaar
Přispěvatelé: Amsterdam institute for Infection and Immunity, Intensive Care Medicine, Amsterdam Cardiovascular Sciences, Anesthesiology
Jazyk: angličtina
Rok vydání: 2010
Předmět:
Zdroj: Anesthesia and analgesia, 111(1), 164-170. Lippincott Williams and Wilkins
ISSN: 0003-2999
Popis: BACKGROUND: S-ketamine is frequently used for analgosedation, especially during sepsis and cardiovascular instability. Because S-ketamine blocks voltage-gated sodium (Na+) channels in neurons and skeletal muscle, it is conceivable that S-ketamine also blocks alveolar epithelial Na+ channels that are crucial for alveolar fluid clearance (AFC). We studied the effects of alveolar and IV S-ketamine on transalveolar Na+ transport and AFC, and investigated whether IV S-ketamine enters the alveolar space in response to endotoxemia-induced pulmonary inflammation. METHODS: Cultured rat alveolar type II (ATII) cells were exposed to S-ketamine and/or the Na+ channel blocker amiloride (100 microM) and transepithelial transport indicated by short circuit current (ISC) was measured in Ussing chambers. AFC was measured in fluid-instilled lungs of anesthetized rats with or without amiloride added to the instillate. S-ketamine was either added to the instillate or injected IV. To induce mild lung injury that might favor the appearance of IV S-ketamine at the alveolar surface, endotoxemia was induced by IV lipopolysaccharide (7.5 mg/kg). RESULTS: In ATII cells, S-ketamine (25 microg/mL) caused a decrease of ISC regardless of apical (-18.9%+/- 1.4%; P
Databáze: OpenAIRE