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      Induction of Heme Oxygenase-1 with Hemoglobin Depresses Vasoreactivity in Rat Aorta

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          Abstract

          Septic shock induced by lipopolysaccharide (LPS) produces systemic hypotension and decreased responsiveness to vasoconstrictors. Recently, intravenous injection of hemoglobin (HGB) into rats was found to be protective from a subsequent lethal dose of LPS and was correlated with induction of the enzyme heme oxygenase-1 (HO-1). To determine whether the HGB modulated the vasomotor tone of systemic arteries, we evaluated the effect of in vivo treatment with HGB and LPS on vasoconstrictor responses to phenylephrine (PE) in the isolated rat aorta. Rats (n = 4, for each group) were injected intravenously with rat HGB (200 mg/kg i.v.) or normal saline control (CON) 16 h before sacrifice, and/or LPS (20 mg/kg) or CON 4 h before sacrifice. The descending aorta was dissected into rings and suspended in a modified Krebs solution where vasoconstrictor responses were determined to KCl (60 m M) and PE (10<sup>–8</sup> to 10<sup>–5</sup> M). LPS, but not HGB, inhibited the vasoconstrictor response to KCl. LPS, HGB, and HGB+LPS inhibited the maximal vasoconstrictor response to PE (PE<sub>max</sub>). Induction of HO-1 RNA in the aorta by HGB and by LPS was demonstrated by Northern blot analysis. To determine if induction of HO-1 was related to the effect of LPS or HGB on vascular reactivity, vessels were treated with the HO-1 inhibitor, SnPP9 (30 μ M). PE<sub>max</sub> in SnPP9+HGB vessels was not different from control, whereas SnPP9+LPS vessels had a marked decrease in PE<sub>max</sub>. We conclude that induction of HO-1 does not protect the rat aorta from the vasodepressor effects of LPS in vitro. Our results demonstrate, however, that the induction of HO-1 causes vasodepression, possibly via increased production of carbon monoxide.

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          Most cited references 3

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          Heme oxygenase 2: endothelial and neuronal localization and role in endothelium-dependent relaxation.

          Heme oxygenase 2 (HO-2), which synthesizes carbon monoxide (CO), has been localized by immunohistochemistry to endothelial cells and adventitial nerves of blood vessels. HO-2 is also localized to neurons in autonomic ganglia, including the petrosal, superior cervical, and nodose ganglia, as well as ganglia in the myenteric plexus of the intestine. Enzyme studies demonstrated that tin protoporphyrin-9 is a selective inhibitor of HO with approximately 10-fold selectivity for HO over endothelial nitric oxide synthase (NOS) and soluble guanylyl cyclase. Inhibition of HO activity by tin protoporphyrin 9 reverses the component of endothelial-derived relaxation of porcine distal pulmonary arteries not reversed by an inhibitor of NOS. Thus, CO, like NO, may have endothelial-derived relaxing activity. The similarity of NOS and HO-2 localizations and functions in blood vessels and the autonomic nervous system implies complementary and possibly coordinated physiologic roles for these two mediators.
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            Desensitization of alpha-1 adrenergic receptor mediated smooth muscle contraction in aorta from endotoxic rats

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              Activation of Soluble Guanylyl Cyclase by a Factor Other Than Nitric Oxide or Carbon Monoxide Contributes to the Vascular Hyporeactivity to Vasoconstrictor Agents in the Aorta of Rats Treated with Endotoxin

               C.C. Wu,  C Szabo,  S.J. Chen (1994)
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                Author and article information

                Journal
                JVR
                J Vasc Res
                10.1159/issn.1018-1172
                Journal of Vascular Research
                S. Karger AG
                1018-1172
                1423-0135
                1999
                April 1999
                22 April 1999
                : 36
                : 2
                : 114-119
                Affiliations
                Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, Md., USA
                Article
                25633 J Vasc Res 1999;36:114–119
                10.1159/000025633
                10213906
                © 1999 S. Karger AG, Basel

                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. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 4, Tables: 2, References: 31, Pages: 6
                Categories
                Research Paper

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