Growth Hormone Treatment in Experimental Heart Failure
During the last years, GH and IGF-I have been recognized as important regulators of cardiac structure and function. The effects of GH on peripheral tissues are thought to be either direct or mediated by IGF-I. IGF-I is synthesized in multiple tissues including the heart and some of the effects have been suggested to be paracrine or autocrine (1-4). Both GH and IGF-I receptors are expressed in the heart and provide possibilities for GH and IGF-I signalling. Importance of the GH/IGF-I axis for the development of cardiac hypertrophy in response to increased hemodynamic load will be discussed in this chapter along with an overview of GH and IGF-I effects on intracellular calcium handling, apoptosis and cardiac performance in various experimental models.
KeywordsCardiac Hypertrophy Growth Hormone Treatment Experimental Myocardial Infarction Experimental Heart Failure Intracellular Calcium Handling
Unable to display preview. Download preview PDF.
- 8.Russell-Jones DL, Leach RM, Ward JPT, Thomas CR. Insulin-like growth factor-I gene expression is increased in the right ventricle hypertrophy induced by chronic hypoxia in the rat. J Endocrinol. 1993;10:99–102.Google Scholar
- 13.Strömer H, Cittadini A, Douglas PS, Morgan JP. Exogenously administered growth hormone and insulin-like growth factor-I alter intracellular Cat+handling and enhance cardiac performance. In vitro evaluation in the isolated isovolumic buffer-perfused rat heart. Circ Res 1996;79:227–236.PubMedCrossRefGoogle Scholar
- 14.Tajima M, Weinberg EO, Bartunek J, et al. Treatment with growth hormone enhances contractile reserve and intracellular calcium transients in myocytes from rats with postinfarction heart failure. Circulation 1999;127–134.Google Scholar
- 27.Narula J, Haider N, Virmani R, et al. Apoptosis in myocytes in end-stage heart failure. N Engl J Med 1996;335–1182-1189.Google Scholar
- 32.Buerke M, Prufer D, Ibe W, et al. Human growth hormone exerts cardioprotective effects in murine reperfusion injury. Abstract # 2116, 70thScientific Session of the American Heart Association, Orlando, November 1997Google Scholar