Skip Navigation

Cardiovascular Research 1998 38(2):500-507; doi:10.1016/S0008-6363(98)00012-1
© 1998 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Deuchar, G. A
Right arrow Articles by MacLean, M. R
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Deuchar, G. A
Right arrow Articles by MacLean, M. R
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 1998, European Society of Cardiology

Pulmonary responses to 5-hydroxytryptamine and endothelin-1 in a rabbit model of left ventricular dysfunction

Graeme A Deuchara, Martin N Hicksa,*, Stuart M Cobbea, Cheryl C Dochertyb and Margaret R MacLeanb

aDepartment of Medical Cardiology, University of Glasgow, Royal Infirmary, Glasgow G31 2ER, UK
bClinical Research Initiative in Heart Failure, Division of Neuroscience and Biomedical Systems, IBLS, West Medical Building, University of Glasgow, Glasgow G12 8QQ, UK

* Corresponding author. Tel.: +44 (141) 211-4860; Fax: +44 (141) 552-4683.

Objective: To determine whether pulmonary hypertension developed in a coronary artery-ligated rabbit model of left ventricular dysfunction (LVD) and to examine the effects of i.v. 5-hydroxytryptamine (5-HT) and endothelin-1 (ET-1) on pulmonary arterial pressure (PAP). Methods: Eight weeks after experimental coronary artery ligation or sham operation, ejection fractions were assessed by echocardiography. The rabbits were later anaesthetised and pulmonary arterial pressure was measured via a catheter inserted into the pulmonary artery via the right external jugular vein. 5-HT (1–400 µg/kg) and ET-1 (0.001–4 nmol/kg) were administered i.v. Results: Ejection fraction was significantly decreased from 76.6±1.4% in sham-operated to 42.2±1.3% in coronary artery-ligated rabbits (n=9 in each group; P<0.001), consistent with LVD. Baseline mean pulmonary arterial pressure was significantly increased in the coronary artery-ligated group compared to the shams, (16.5±0.5 vs. 11.5±0.8 mmHg; P<0.001). A significant degree of right ventricular hypertrophy was found in the coronary artery-ligated rabbits (0.70±0.04 g/kg final body weight (f.b.wt.), n=8 cf. 0.48±0.02 g/kg f.b.wt. in sham-operated controls, n=8; P<0.001). There was a significant increase in the percentage of muscularised pulmonary vessels adjacent to alveolar ducts and alveoli <60 µm i.d. in the LVD rabbits compared with their sham-operated controls (8.5±0.4 cf. 20±0.5%; P<0.0005). 5-HT produced a greater response in the coronary artery-ligated rabbits (a maximum increase of 8.7±1.0 mmHg in mean pulmonary artery pressure vs. 4.6±1.5 mmHg for sham-operated controls; P<0.05). ET-1 did not have any effect on pulmonary arterial pressure in either group. Conclusion: In the rabbit, LVD secondary to coronary artery ligation, causes right ventricular hypertrophy, pulmonary vascular remodelling, and an increased PAP consistent with the onset of pulmonary hypertension (PHT). The greater PAP response to i.v. 5-HT in the PHT group supports the hypothesis that this substance could be involved in the development of PHT. A role for ET-1 cannot be excluded, despite its lack of effect on PAP when intravenously administered in either group.

KEYWORDS Pulmonary Hypertension; 5-hydroxytryptamine; Endothelin; Left ventricular dysfunction; Rabbit


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 HypertensionHome page
I. Morecroft, Y. Dempsie, M. Bader, D. J. Walther, K. Kotnik, L. Loughlin, M. Nilsen, and M. R. MacLean
Effect of Tryptophan Hydroxylase 1 Deficiency on the Development of Hypoxia-Induced Pulmonary Hypertension
Hypertension, January 1, 2007; 49(1): 232 - 236.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
M. Nahrendorf, K. Hu, D. Fraccarollo, K.-H. Hiller, A. Haase, W. R. Bauer, and G. Ertl
Time course of right ventricular remodeling in rats with experimental myocardial infarction
Am J Physiol Heart Circ Physiol, January 1, 2003; 284(1): H241 - H248.
[Abstract] [Full Text] [PDF]

Home page
 ThoraxHome page
Poster presentations
Thorax, December 1, 2002; 57(90003): iii48 - 94.
[Full Text] [PDF]

Home page
 Cardiovasc ResHome page
W. Huang, M. P Kingsbury, M. A Turner, J.L. Donnelly, N. A Flores, and D. J Sheridan
Capillary filtration is reduced in lungs adapted to chronic heart failure: morphological and haemodynamic correlates
Cardiovasc Res, January 1, 2001; 49(1): 207 - 217.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
A. Keegan, I. Morecroft, D. Smillie, M. N. Hicks, and M. R. MacLean
Contribution of the 5-HT1B Receptor to Hypoxia-Induced Pulmonary Hypertension: Converging Evidence Using 5-HT1B-Receptor Knockout Mice and the 5-HT1B/1D-Receptor Antagonist GR127935
Circ. Res., December 7, 2001; 89(12): 1231 - 1239.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.