JOURNAL HOME CME HOME THIS MONTH PAST ISSUES ETOC COLLECTIONS AUTHORS REVIEWERS EDITORIAL BOARD FEEDBACK RSS HELP
		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Kerbaul, F. Articles by Naeije, R. Search for Related Content PubMed PubMed Citation Articles by Kerbaul, F. Articles by Naeije, R. Related Collections Complications Cardiovascular Critical Care Airway

---

CRITICAL CARE AND TRAUMA

Prevention of Hemodilution-Induced Inhibition of Hypoxic Pulmonary Vasoconstriction by N-Acetylcysteine in Dogs

François Kerbaul, MD^*, Philippe Van der Linden, MD PhD, Sébastien Pierre, MD, Benoît Rondelet, MD, Christian Melot, MD PhD, Serge Brimioulle, MD PhD, and Robert Naeije, MD PhD

*Department of Anesthesia and Intensive Care, Timone Hospital, Marseille, France; Department of Anesthesia, Centre Hospitalo-Universitaire, Charleroi, Belgium; Department of Physiology, Faculty of Medicine, Free University of Brussels, Brussels, Belgium; and Department of Intensive Care, Erasme Hospital, Free University of Brussels, Belgium

Address correspondence and reprint requests to Robert Naeije, MD, Department of Physiology, Erasme Campus CP 604, 808, Lennik Rd., B-1070 Brussels, Belgium. Address e-mail to rnaeije{at}ulb.ac.be

We investigated the possible contributions of reactive oxygen species and of viscosity changes to hemodilution-induced inhibition of hypoxic pulmonary vasoconstriction (HPV) in dogs. Fourteen isoflurane-anesthetized dogs were randomly assigned to receive N-acetylcysteine (NAC) 200 mg/kg IV (n = 7) or placebo (n = 7). Mean pulmonary artery pressure (Ppa) was measured with cardiac output maintained constant by a manipulation of venous return in hyperoxia (fraction of inspired oxygen, 0.4) and in hypoxia (fraction of inspired oxygen, 0.1) at baseline and after stepwise reductions in hematocrit from 40% to 20%. Measured Ppa was compared with predicted Ppa by using a viscoelastic model. HPV was expressed as hypoxic Ppa minus hyperoxic Ppa. Hemodilution was associated with a decrease in HPV from 7 ± 1 mm Hg to 3 ± 1 mm Hg (P < 0.01), and this was completely prevented by NAC (HPV was unchanged, from 8 ± 1 to 8 ± 1 mm Hg; not significant). Hemodilution in the model decreased HPV from 8 ± 1 mm Hg to 6 ± 1 mm Hg (P < 0.05). We conclude that hemodilution-induced inhibition of HPV is in part explained by viscosity changes and can be prevented by the administration of NAC, which is possibly explained by the scavenging of reactive oxygen species.

IMPLICATIONS: Hemodilution inhibits hypoxic pulmonary vasoconstriction. This study showed that this potential cause of altered gas exchange is partly explained by viscosity changes and is completely preventable by the administration of the reactive oxygen species scavenger N-acetylcysteine.

Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999