Hostname: page-component-586b7cd67f-l7hp2 Total loading time: 0 Render date: 2024-11-23T02:54:43.777Z Has data issue: false hasContentIssue false
  • English
  • Français

Age is a risk factor for maladaptive changes in rats exposed to increased pressure loading of the right ventricular myocardium

Published online by Cambridge University Press:  23 March 2007

Vladimiro L. Vida ,
Annalisa Angelini ,
Simonetta Ausoni ,
Alessandra Bilardi ,
Carlo Ori ,
Francesca Vlassich ,
Valentina Zoso ,
Ornella Milanesi ,
Saverio Sartore  and
Mila della Barbera
...Show all authors
Vladimiro L. Vida
Affiliation:
Department of Pediatric Cardiac Surgery, University of Padua, Italy
Annalisa Angelini
Affiliation:
Department of Pathology, University of Padua, Italy
Simonetta Ausoni
Affiliation:
Department of Biomedical Sciences, University of Padua, Italy
Alessandra Bilardi
Affiliation:
Department of Biomedical Sciences, University of Padua, Italy
Carlo Ori
Affiliation:
Department of Anesthesia, University of Padua, Italy
Francesca Vlassich
Affiliation:
Department of Anesthesia, University of Padua, Italy
Valentina Zoso
Affiliation:
Department of Anesthesia, University of Padua, Italy
Ornella Milanesi
Affiliation:
Department of Pediatrics, University of Padua, Italy
Saverio Sartore
Affiliation:
Department of Biomedical Sciences, University of Padua, Italy
Mila della Barbera
Affiliation:
Department of Pathology, University of Padua, Italy
Tania Zaglia
Affiliation:
Department of Biomedical Sciences, University of Padua, Italy
Gaetano Thiene
Affiliation:
Department of Pathology, University of Padua, Italy
Giovanni Stellin
Affiliation:
Department of Pediatric Cardiac Surgery, University of Padua, Italy
Get access Rights & Permissions [Opens in a new window]

Abstract

Objective: To study the adaptive potential of the right ventricular myocardium after 30 days of mechanical-induced overload in rats from two different age groups. Materials and methods: We banded the pulmonary trunk, so as to increase the systolic work load of the right ventricle, in 19 adult Sprague-Dawley rats at the age of 10 weeks, and 16 weanlings when they were 3 weeks-old, using 10 adults and 10 weanlings as controls. We analysed the functional adaptation and structural changes of the right ventricular myocardium, blood vessels and interstitial tissue after 30 days of increased afterload. Results: The increased workload induced an increase of the right ventricular weight and free wall thickness in animals from both age groups when compared to controls. These changes were mostly related to cardiomyocytic hypertrophy, as confirmed by the expression of myocardial hypertrophic markers, without any apparent increase of their number, a “reactive” fibrosis especially evident in the adult rats, with p-value less than 0.0001, and a more extensive neocapillary network in the weanlings compared to the adults aubsequent to banding, the p-value being less than 0.0001. Conclusion: In response to right ventricular afterload, weanlings showed a higher adaptive capillary growth, which hampered the development of fibrosis as seen in the adult rats. Age seems to be a risk factor for adverse structural-functional changes of right ventricle subjected to increased workload.

Keywords

Heart failureremodelingcongenital defectsventricular functionextra-cellular matrix
Type
Original Article
Information
Cardiology in the Young , Volume 17 , Issue 2 , April 2007 , pp. 202 - 211
Copyright
© 2007 Cambridge University Press

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Wells WJ, Blackstone E. Intermediate outcome after Mustard and Senning procedures: A study by the Congenital Heart Surgeons Society. Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu 2000; 3: 186–197.Google Scholar
Duncan BW, Mee RB. Management of the failing systemic right ventricle. Semin Thorac Cardiovasc Surg 2005; 17: 160–169.Google Scholar
Brawn WJ. The double switch for atrioventricular discordance. Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu 2005; 8: 51–56.Google Scholar
Gorenflo M, Serpi M, Schnabel PA, et al. Pathological changes of the myocardium in patients after atrial repair for transposition of the great arteries: a possible explanation for left ventricular dysfunction after secondary arterial switch. Z Kardiol 2003; 92: 742–746.Google Scholar
Rentzsch A, Abd El Rahman MY, Hui W, et al. Assessment of myocardial function of the systemic right ventricle in patients with D-transposition of the great arteries after atrial switch operation by tissue Doppler echocardiography. Z Kardiol 2005; 94: 524–531.Google Scholar
Singh TP, Humes RA, Muzik O, Kottamasu S, Karpawich PP, Di Carli MF. Myocardial flow reserve in patients with a systemic right ventricle after atrial switch repair. J Am Coll Cardiol 2001; 37: 2120–2125.Google Scholar
Millane T, Bernard EJ, Jaeggi E, et al. Role of ischemia and infarction in late right ventricular dysfunction after atrial repair of transposition of the great arteries. J Am Coll Cardiol 2000; 35: 1661–1668.Google Scholar
Schaub MC, Hefti MA, Harder BA, Eppenberger HM. Various hypertrophic stimuli induce distinct phenotypes in cardiomyocytes. J Mol Med 1997; 75: 901–920.Google Scholar
Clement S, Chaponnier C, Gabbiani G. A subpopulation of cardiomyocytes expressing alpha-skeletal actin is identified by a specific polyclonal antibody. Circ Res 1999; 85 (10): e51–e58.Google Scholar
Glantz S. Primer of biostatistics. Fifth ed. McGraw-Hill, United States, 2002.
Konarzewska H, Peeters GA, Sanguinetti MC. Repolarizing K+ currents in nonfailing human hearts. Similarities between right septal subendocardial and left subepicardial ventricular myocytes. Circulation 1995; 92: 1179–1187.Google Scholar
Urbanek K, Quaini F, Tasca G, et al. Intense myocyte formation from cardiac stem cells in human cardiac hypertrophy. Proc Natl Acad Sci USA 2003; 100: 10440–10445.Google Scholar
Li F, Wang X, Capasso JM, Gerdes AM. Rapid transition of cardiac myocytes from hyperplasia to hypertrophy during postnatal development. J Mol Cell Cardiol 1996; 26: 1737–1746.Google Scholar
Schmid P, Jaermann T, Boesiger P, et al. Ventricular myocardial architecture as visualised in postmortem swine hearts using magnetic resonance diffusion tensor imaging. Eur J Cardiothorac Surg 2005; 27: 468–472.Google Scholar
Anderson RH, Ho SY, Redmann K, Sanchez-Quintana D, Lunkenheimer PP. The anatomical arrangement of the myocardial cells making up the ventricular mass. Eur J Cardiothorac Surg 2005; 28: 517–525.Google Scholar
Lunkenheimer PP, Redmann K, Anderson RH. Further discussions concerning the unique myocardial band. Eur J Cardiothorac Surg 2005; 28: 779–780.Google Scholar
Manabe I, Shindo T, Nagai R. Gene expression in fibroblasts and fibrosis. Circ Res 2002; 91: 1103–1113.Google Scholar
Ikeda S, Hamada M, Hiwada K. Cardiomyocyte apoptosis with enhanced expression of P53 and Bax in right ventricle after pulmonary arterial banding. Life Sci 1999; 65: 925–933.Google Scholar
Harada K, Komuro I, Shiojima I, et al. Pressure overload induces cardiac hypertrophy in angiotensin II type 1A receptor knockout mice. Circulation 1998; 97: 1952–1959.Google Scholar
Carnes CA, Geisbuhler TP, Reiser PJ. Age-dependent changes in contraction and regional myocardial myosin heavy chain isofrom expression in rats. J Appl Physiol 2004; 97: 446–453.Google Scholar
Lekanne Deprez RH, van den Hoff MJ, de Boer PA, et al. Changing patterns of gene expression in the pulmonary trunk-banded rat heart. J Mol Cell Cardiol 1998; 30: 1877–1888.Google Scholar