Myocardial function in different models of cardiac hypertrophy. An attempt at correlating mechanical, biochemical, and morphological parameters

Abstract

Based on mechanical, biochemical and electron microscopic studies performed in the same stage of experimental cardiac hypertrophy, an attempt is made to define the significance of individual factors responsible for the alterations in myocardial function. Using swimming rats, it is demonstrated that a load-induced increase in cardiac mass is not necessarily connected with an impairment of contractile capability on a cellular level. Yet, also, the reduction of specific ATPase activity and unloaded shortening velocity in pressure-induced hypertrophy (goldblatt rats; aortic stenosis) seems to be the expression of adaptation rather than of cellular damage, at least in the earlier stages. Although there are distinct indications of alterations in Ca-dependent activation and deactivation, in the Goldblatt model electromechanical coupling does not seem to be the main cause of altered contraction parameters. The correlation between specific ATPase activity of actomyosin and unloaded shortening velocity as well as the persistance of decrease in shortening velocity, also under optimal electromechanical coupling conditions, point to an inner relationship between the two values. A discrepancy between unloaded shortening velocity on the one hand and developed tension on the other is mainly due to an increased content of contractile structures. In later stages, an increased connective tissue content influences both isometric and isotonic parameters.

Myocardial collagen in different forms of heart hypertrophy in the rat

“…in left ventricular tissue of Goldblatt rats at an early stage (up to 6 weeks after surgery) is to be expected in different experimental groups. Our previous study [11] demonstrated that ventricular contractile capability can be increased in this phase of cardiac hypertrophy, as an expression of adaptation to increased functional requirements.…”

Cardiac conditioning ameliorates cardiac dysfunction associated with renal hypertension in rats.

“…This report confirms that Tables I and II. cardiac hypertrophy due to renal hypertension in rats is associated with a depressed coronary reserve (7,17) and diminished contractile performance ofthe left ventricle (4)(5)(6)(7). These results contrast with our previous findings ofimproved contractile performance in hypertrophied hearts from female rats trained by a chronic swimming program (12).…”

“…Half of the animals in the control and hypertensive groups were subjected to a swimming program and the other half remained cage-confined (sedentary). The exercise program, described previously (1 1-13), consisted of swimming 5 d/wk, 75 min twice a day for 10 wk. At the completion of this period, exercised and sedentary animals were anesthetized with ether, their hearts were removed and studied in the isolated working rat heart apparatus.…”

“…In the first series ofexperiments hearts were perfused for analysis of pump function, myocardial function, and cardiac metabolism. Full descriptions of the isolated working rat heart apparatus have been published previously (1 [1][2][3][4][5][6][7][8][9][10][11][12][13]. The Cardiac function was assessed at two levels of preload at each of three levels of afterload.…”

“…However, in rats this is generally associated with depressed myocardial contractility and ventricular function (4)(5)(6)(7). On the other hand, hypertrophy associated with hyperthyroidism or with physical training has frequently been found to be associated with enhanced myocardial contractile performance and ventricular function (8).…”