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 Google Scholar Google Scholar Articles by Debarge, V. H. Articles by Storme, L. Search for Related Content PubMed PubMed Citation Articles by Debarge, V. H. Articles by Storme, L. Related Collections Mechanisms Pediatrics Pain

---

PEDIATRIC ANESTHESIA

The Mechanisms of Pain-Induced Pulmonary Vasoconstriction: An Experimental Study in Fetal Lambs

Veronique Houfflin Debarge, MD, PhD^*, Bérengère Sicot, MD^*, Sophie Jaillard, MD, PhD, Iva Gueorgiva, MD, Anne Delelis, MD^*, P. Deruelle, MD, PhD^*, Ann Sophie Ducloy, MD^||, and Laurent Storme, MD

From the *Department of Obstetrics, Centre Hospitalier Régional Universitaire, Lille, France; JE 2490 and Departement Hospitalo-Universitaire de Recherche Experimentale, Faculté de Médecine de Lille, Université de Lille II, Lille, France; and Departments of Neonatology and ||Anesthesiology, Centre Hospitalier Régional Universitaire, Lille, France.

Address correspondence to Véronique Houfflin Debarge, MD, Clinique d'Obstétrique, Hôpital Jeanne de Flandre, Centre Hospitalier Régional et Universitaire, 59037 Lille Cedex, France. Address e-mail to v-houfflin-debarge{at}chru-lille.fr.

BACKGROUND: Nociceptive stimulation induces pulmonary vasoconstriction in fetuses and newborns. The mechanism of this response is not fully understood. As the systemic hemodynamic response to pain is mainly mediated by sympathetic stimulation, we hypothesized that pain-induced pulmonary vasoconstriction results from the activation of catecholaminergic receptors. To test this hypothesis, we studied the pulmonary vascular response to nociceptive stimuli in fetal lambs before and after -adrenoceptor blockade.

METHODS: Surgery was performed in fetal lambs. Catheters were placed into the ascending aorta, superior vena cava, and main pulmonary artery. An ultrasonic flow transducer was placed around the left pulmonary artery, and subcutaneous catheters were placed in the limb. The hemodynamic responses to (1) subcutaneous injection of formalin (which is used as nociceptive stimulus in experimental studies), (2) prazosin (specific ₁-adrenoceptor antagonist), and (3) formalin during prazosin infusion were evaluated. Plasma cortisol and catecholamine concentrations were measured.

RESULTS: Pulmonary vascular resistance (PVR) increased by 50% (P < 0.01) after the formalin test. PVR did not change after the formalin test during prazosin infusion or during prazosin infusion alone. Catecholamine and cortisol levels did not change during any of the protocols.

DISCUSSION: Our results indicate that the fetal pulmonary vasoconstrictive response to pain involves ₁-adrenoceptors activation. As plasma catecholamine concentrations did not change after the formalin test, we speculate that the pulmonary vascular response to nociceptive stimuli could be triggered by a local release of catecholamine induced by sympathetic stimulation.

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