Summary
In response to an increased afterload, the myocardium undergoes a complex adaptation by which wall stress is normalized and cardiac output is maintained. Although the consensus suggests that the increase of the myocardial mass is a necessary adaptive process to accommodate the increased workload, there is growing evidence that hypertrophy ultimately results in pathological remodeling and deterioration of cardiac function. Despite intense investigation, our understanding of the cellular mechanisms that are responsible for the initiation and the maintenance of this adaptation is largely incomplete and preventing or regressing left ventricular hypertrophy (LVH) is a major challenge. This chapter provides a detailed description of the procedures necessary to induce LVH by coarctation of the transverse aorta and to analyze the effects of the increased hemodynamic load on cardiac mass, cardiomyocyte size, and cardiac performance.
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References
Engelhardt, S., Hein, L., Wiesmann, F., and Lohse, M.J. (1999) Progressive hypertrophy and heart failure in β 1-adrenergic receptor transgenic mice. Proc. Natl. Acad. Sci. U. S. A. 96, 7059–7064.
Liggett, S.B., Tepe, N.M., Lorenz, J.N., Canning, A.M., Jantz, T.D., Mitarai, S., et al. (2000) Early and delayed consequences of β 2-adrenergic receptor overexpression in mouse hearts: critical role for expression level. Circulation 101, 1707–1714.
Kohout, T.A., Takaoka, H., McDonald, P.H., Perry, S.J., Mao, L., Lefkowitz, R.J., et al. (2001) Augmentation of cardiac contractility mediated by the human β 3-adrenergic receptor overexpressed in the hearts of transgenic mice. Circulation 104, 2485–2491.
Iwase, M., Bishop, S.P., Uechi, M., Vatner, D.E., Shannon, R.P., Kudej, R.K., et al. (1996) Adverse effects of chronic endogenous sympathetic drive induced by cardiac Gsα overexpression. Circ. Res. 78, 517–524.
Antos, C.L., Frey, N., Marx, S.O., Reiken, S., Gaburjakova, M., Richardson, J.A., et al. (2001) Dilated cardiomyopathy and sudden death resulting from constitutive activation of protein kinase a. Circ. Res. 89, 997–1004.
Du, X.J., Autelitano, D.J., Dilley, R.J., Wang, B., Dart, A.M., and Woodcock, E.A. (2000) β 2-adrenergic receptor overexpression exacerbates development of heart failure after aortic stenosis. Circulation 101, 71–77.
Rapacciuolo, A., Esposito, G., Caron, K., Mao, L., Thomas, S.A., and Rockman, H.A. (2001) Important role of endogenous norepinephrine and epinephrine in the development of in vivo pressure-overload cardiac hypertrophy. J. Am. Coll. Cardiol. 38, 876–882.
Palazzesi, S., Musumeci, M., Catalano, L., Patrizio, M., Stati, T., Michienzi, S., et al. (2006) Pressure overload causes cardiac hypertrophy in beta1-adrenergic and beta2-adrenergic receptor double knockout mice. J. Hypertens. 24, 563–571.
Milano, C.A., Dolber, P.C., Rockman, H.A., Bond, R.A., Venable, M.E., Allen, L.F., et al. (1994) Myocardial expression of a constitutively active alpha 1B-adrenergic receptor in transgenic mice induces cardiac hypertrophy. Proc. Natl. Acad. Sci. U. S. A. 91, 10109–10113.
Brede, M., Wiesmann, F., Jahns, R., Hadamek, K., Arnolt, C., Neubauer, S., et al. (2002) Feedback inhibition of catecholamine release by two different alpha2-adrenoceptor subtypes prevents progression of heart failure. Circulation 106, 2491–2496.
O’Connell, T.D., Swigart, P.M., Rodrigo, M.C., Ishizaka, S., Joho, S., Turnbull, L., et al. (2006) Alpha1-adrenergic receptors prevent a maladaptive cardiac response to pressure overload. J. Clin. Invest. 116, 1005–1015.
Perlini, S., Palladini, G., Ferrero, I., Tozzi, R., Fallarini, S., Facoetti, A., et al. (2005) Sympathectomy or doxazosin, but not propranolol, blunt myocardial interstitial fibrosis in pressure-overload hypertrophy. Hypertension 46, 1213–1218.
Perlini, S., Ferrero, I., Palladini, G., Tozzi, R., Gatti, C., Vezzoli, M., et al. (2006) Survival benefits of different antiadrenergic interventions in pressure overload left ventricular hypertrophy/failure. Hypertension 48, 93–97.
Costa, D.L., Lehmann, J.R., Harold, W.M., and Drew, R.T. (1986) Transoral tracheal intubation of rodents using a fiberoptic laryngoscope. Lab. Anim. Sci. 36, 256–261.
Brown, R.H., Walters, D.M., Greenberg, R.S., and Mitzner, W. (1999) A method of endotracheal intubation and pulmonary functional assessment for repeated studies in mice. J. Appl. Physiol. 87, 2362–2365.
Vergari, A., Polito, A., Musumeci, M., Palazzesi, S., and Marano, G. (2003) Video-assisted orotracheal intubation in mice. Lab. Anim. 37, 204–206.
Rockman, H.A., Ross, R.S., Harris, A.N., Knowlton, K.U., Steinhelper, M.E., Field, L.J., et al. (1991) Segregation of atrial-specific and inducible expression of an atrial natriuretic factor transgene in an in vivo murine model of cardiac hypertrophy. Proc. Natl. Acad. Sci. U. S. A. 88, 8277–8281.
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Marano, G., Ferrari, A.U. (2007). Surgical Animal Model of Ventricular Hypertrophy. In: Sreejayan, N., Ren, J. (eds) Vascular Biology Protocols. Methods in Molecular Medicine™, vol 139. Humana Press. https://doi.org/10.1007/978-1-59745-571-8_5
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DOI: https://doi.org/10.1007/978-1-59745-571-8_5
Publisher Name: Humana Press
Print ISBN: 978-1-58829-574-3
Online ISBN: 978-1-59745-571-8
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