|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Cardiology, Leiden University Medical Center, Leiden, Netherlands
* To whom correspondence should be addressed. E-mail: p.steendijk{at}lumc.nl.
We characterized hemodynamics and systolic and diastolic right ventricular (RV) function in relation to structural changes in the rat model of monocrotaline (MCT)-induced pulmonary hypertension. Rats were treated with 30 mg/kg (MCT30, n=15) or 80 mg/kg (MCT80, n=16) MCT to induce compensated RV hypertrophy or RV failure, respectively. Saline-treated rats served as control (CONT, n=13). After 4 weeks, a pressure-conductance catheter was introduced into the RV to assess pressure-volume relations. Subsequently, rats were sacrificed, hearts and lungs were rapidly dissected, and RV, left ventricle (LV) and interventricular septum (IVS) were weighed and analyzed histochemically. RV/(LV+IVS) weight ratio was 0.29±0.05 in CONT, 0.35±0.05 in MCT30 and 0.49±0.10 in MCT80 rats (p<0.001 vs. CONT and MCT30) confirming MCT-induced RV hypertrophy. RV ejection fraction was 49±6% in CONT, 40±12% in MCT30 (p<0.05 vs. CONT) and 26±6% in MCT80 rats (p<0.05 vs. CONT and MCT30). In MCT30 rats, cardiac output was maintained, but RV volumes and filling pressures were significantly increased compared to CONT (all p<0.05), indicating RV remodeling. In MCT80 rats, RV systolic pressure, volumes and peak wall stress were further increased, and cardiac output was significantly decreased (all p<0.05). However, RV end-systolic and end-diastolic stiffness were unchanged, consistent with the absence of interstitial fibrosis. MCT-induced pressure-overload was associated with a dose-dependent development of RV hypertrophy. The most pronounced response to MCT was an overload-dependent increase of RV end-systolic and end-diastolic volumes, even under non-failing conditions.
This article has been cited by other articles:
![]() |
S. Umar, Y. P. de Visser, P. Steendijk, C. I. Schutte, E. H. Laghmani, G. T. M. Wagenaar, W. H. Bax, E. Mantikou, D. A. Pijnappels, D. E. Atsma, et al. Allogenic stem cell therapy improves right ventricular function by improving lung pathology in rats with pulmonary hypertension Am J Physiol Heart Circ Physiol, November 1, 2009; 297(5): H1606 - H1616. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Gur, P. J. Kadowitz, S. Thammasitboon, J. A. Lasky, and W. J. G. Hellstrom Characterization of Erectile Function in Monocrotaline-Treated Pulmonary Hypertensive Rats J Androl, September 1, 2009; 30(5): 495 - 504. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Yamazato, A. J. Ferreira, K.-H. Hong, S. Sriramula, J. Francis, M. Yamazato, L. Yuan, C. N. Bradford, V. Shenoy, S. P. Oh, et al. Prevention of Pulmonary Hypertension by Angiotensin-Converting Enzyme 2 Gene Transfer Hypertension, August 1, 2009; 54(2): 365 - 371. [Abstract] [Full Text] [PDF] |
||||
![]() |
M.L. Handoko, F.S. de Man, C.M. Happe, I. Schalij, R.J.P. Musters, N. Westerhof, P.E. Postmus, W.J. Paulus, W.J. van der Laarse, and A. Vonk-Noordegraaf Opposite Effects of Training in Rats With Stable and Progressive Pulmonary Hypertension Circulation, July 7, 2009; 120(1): 42 - 49. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. Pokreisz, G. Marsboom, and S. Janssens Pressure overload-induced right ventricular dysfunction and remodelling in experimental pulmonary hypertension: the right heart revisited Eur. Heart J. Suppl., December 1, 2007; 9(suppl_H): H75 - H84. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. R. Lamberts, E. Caldenhoven, M. Lansink, G. Witte, R. J. Vaessen, J. A. St Cyr, and G. J. M. Stienen Preservation of diastolic function in monocrotaline-induced right ventricular hypertrophy in rats Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1869 - H1876. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |