European Surgical Research
Original Paper
PGI2 Aerosol versus Nitric Oxide for Selective Pulmonary Vasodilation in Hypoxic Pulmonary VasoconstrictionWelte M.a · Zwissler B.a · Habazettl H.b · Messmer K.baInstitute of Anaesthesiology and bInstitute for Surgical Research, University of Munich, FRG
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Article / Publication Details
Received: February 08, 1993
Accepted: June 04, 1993
Published online: April 23, 2008
Issue release date: 1993
Number of Print Pages: 12
Number of Figures: 0
Number of Tables: 0
ISSN: 0014-312X (Print)
eISSN: 1421-9921 (Online)
For additional information: https://www.karger.com/ESR
Abstract
Intravenous prostacyclin (PGI2) is a potent pulmonary vasodilator in pulmonary hypertension. However, dose-dependent systemic vasodilation, an increase in intrapulmonary shunt and hypoxemia limit its clinical application. Recently, inhaled nitric oxide (NO) has been reported to elicit selective pulmonary vasodilation, but its clinical use is restricted by its potential toxicity; furthermore, the feasibility of NO application in clinical practice seems difficult. Therefore, we investigated the effects of PGI2 aerosol on pulmonary and systemic circulation and compared the hemodynamic effects to those of inhaled NO. In 6 dogs, ventilation with a hypoxic gas mixture (F102 0.09–0.11) increased pulmonary vascular resistance (PVR) by 196% (HPV). Aerosolization of a PGI2 solution at a concentration of 430 ng/ml reduced hypoxia-induced increase of pulmonary artery pressure by 48% and PVR by 52% within 6-10 min without systemic vasodilation. The administered dose of PGI2 was 0.87 ± 0.26 ng/kg/min. In 2 dogs, doubling the PGI2 concentration (860 ng/ml) did not enhance the vasodilatory effect. After termination of PGI2 inhalation, HPV was restored within 10–15 min. Inhaled NO (50 ppm) decreased the HPV-induced increase in PAP by 76% and in PVR by 73% within 5-10 min. Clinically relevant systemic vasodilation was not observed. It is concluded that inhalation of aerosolized PGI2 leads to selective pulmonary vasodilation in hypoxia-induced pulmonary hypertension. Aerosolized PGI2 at a concentration of 430 ng/ml was less potent than NO (50 ppm). However, due to the lack of known toxicity and its uncomplicated mode of application, inhaled PGI2 may be one alternative to inhaled NO in the treatment of acute pulmonary hypertension.
© 1993 S. Karger AG, Basel
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Article / Publication Details
Received: February 08, 1993
Accepted: June 04, 1993
Published online: April 23, 2008
Issue release date: 1993
Number of Print Pages: 12
Number of Figures: 0
Number of Tables: 0
ISSN: 0014-312X (Print)
eISSN: 1421-9921 (Online)
For additional information: https://www.karger.com/ESR
Copyright / Drug Dosage / Disclaimer
Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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