caa a22 4500 46794234X CHVBK 20180406153016.0 cr unu---uuuuu 170328e20060501xx s 000 0 eng 10.1007/s00421-006-0179-8 doi (NATIONALLICENCE)springer-10.1007/s00421-006-0179-8 Increased expired NO and roles of CO2 and endogenous NO after venous gas embolism in rabbits [Elektronische Daten] [Per Agvald, L. Adding, Kristofer Nilsson, Lars Gustafsson, Dag Linnarsson] Venous gas embolism (VGE) is a feared complication in diving, aviation, surgery and trauma. We hypothesized that air emboli in the lung circulation might change expired nitric oxide (FeNO). A single intravenous infusion of air was given (100μlkg−1) to three groups of anaesthetized mechanically ventilated rabbits: (A) one with intact NO production, (B) one with intact NO production and where end-tidal CO2 was controlled, and (C) one with endogenous NO synthesis blockade (l-NAME, 30mgkg−1). Air infusions resulted in increased FeNO of the control group from 20 (4) [mean (SD)] ppb to a peak value of 39 (4)ppb within 5min (P < 0.05), and FeNO was still significantly elevated [27 (2) ppb] after 20min (P<0.05). Parallel to the NO increase there were significant decreases in end-tidal CO2 (ETCO2) and mean arterial pressure and an increase in insufflation pressure. In group B, when CO2 was supplemented after air infusion, NO was suppressed (P=0.033), but was still significantly elevated compared with pre-infusion control (P<0.05). In group C, all animals died within 40min of air infusion whereas all animals in the other groups were still alive at this time point. We conclude that venous air embolization increases FeNO, and that a part of this effect is due to the concomitant decrease in ETCO2. Furthermore, an intact NO production may be critical for the tolerance to VGE. Finally, FeNO might have a potential in the diagnosis and monitoring of pulmonary gas embolism. Springer-Verlag, 2006 Respiratory system nationallicence Pulmonary circulation nationallicence Exhaled nitric oxide nationallicence Decompression sickness nationallicence Hyperbaric medicine nationallicence Agvald Per Department of Physiology and Pharmacology, Karolinska Institutet, 17177, Stockholm, Sweden aut Adding L. Department of Physiology and Pharmacology, Karolinska Institutet, 17177, Stockholm, Sweden aut Nilsson Kristofer Department of Physiology and Pharmacology, Karolinska Institutet, 17177, Stockholm, Sweden aut Gustafsson Lars Department of Physiology and Pharmacology, Karolinska Institutet, 17177, Stockholm, Sweden aut Linnarsson Dag Department of Physiology and Pharmacology, Karolinska Institutet, 17177, Stockholm, Sweden aut European Journal of Applied Physiology Springer-Verlag 97/2(2006-05-01), 210-215 1439-6319 97:2<210 2006 97 421 https://doi.org/10.1007/s00421-006-0179-8 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00421-006-0179-8 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Agvald Per Department of Physiology and Pharmacology, Karolinska Institutet, 17177, Stockholm, Sweden aut NATIONALLICENCE 700 1- Adding L. Department of Physiology and Pharmacology, Karolinska Institutet, 17177, Stockholm, Sweden aut NATIONALLICENCE 700 1- Nilsson Kristofer Department of Physiology and Pharmacology, Karolinska Institutet, 17177, Stockholm, Sweden aut NATIONALLICENCE 700 1- Gustafsson Lars Department of Physiology and Pharmacology, Karolinska Institutet, 17177, Stockholm, Sweden aut NATIONALLICENCE 700 1- Linnarsson Dag Department of Physiology and Pharmacology, Karolinska Institutet, 17177, Stockholm, Sweden aut NATIONALLICENCE 773 0- European Journal of Applied Physiology Springer-Verlag 97/2(2006-05-01), 210-215 1439-6319 97:2<210 2006 97 421 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer