Relation of Increase in Muscle Mass to Performance of Hypertrophied Right Ventricle in the Dog

SUMMARY To evaluate cardiac performance in renal hypertension more precisely we determined cardiac function curves for 12 normotensive rats and 11 other rats with two-kidney Goldblatt hypertension. The hypertensive group (BP = 134 ± 8 mm Hg) showed significant cardiac hypertrophy (44 ± 1% increased ratio of heart weight to body weight, P < 0.01) and markedly increased left ventricular stroke work with a moderate but not significant increase in left ventricular end-diastolic pressure (LVEDP) (5.9 ± 0.8 vs. CARDIAC hypertrophy generally has been considered one of the principal long-term mechanisms of compensation for cardiac stress; 1 the increase in cardiac mass is believed to make the heart as strong a pump as it had been previously. It is known that the increase in contractile strength which follows hypertrophy is due to an increase in muscle mass and that the strength of individual muscle fibers remains unchanged or even may decrease slightly. 2 ' 7 The influence of myocardial hypertrophy on the performance of the hypertensive heart is of particular interest because cardii.c hypertrophy frequently accompanies arterial hypertension and it has been pointed out that early hypertension, in both man and animals, is associated with an increased cardiac output and signs of a hyperkinetic circulation. 8 " 11 The relationship of the increased cardiac output to the development of cardiac hypertrophy has yet to be investigated. Recent studies which show an increased cardiac contractility during the onset of renal hypertension 12 and the early development of cardiac hypertrophy in two forms of hypertension 13 -14 suggest a causal relationship between increased cardiac output and development of cardiac hypertrophy.With the advent of refinements in microtransducer technology it has become possible to accurately measure cardiac output and arterial and venous pressures in small mammals with and without arterial hypertension and thus evaluate cardiac performance in a precise manner. Further, correlation of hemodynamic alterations with biochemical changes which characterize the type of hypertrophy should open the way for a better understanding of cardiac mechanics. To our knowledge this has not been attempted before in hypertensive heart disease, nor is there direct information on the effects of cardiac hypertrophy on ventricular function curves (see Reference 15 for review). We therefore studied the functional link between the appearance of cardiac hypertrophy and the performance of the heart in rats with chronic renal hypertension. MethodsWe performed experiments on 20 normal Wistar rats and on 14 rats with sustained renal hypertension (average duration, 9 weeks; range, 6-22 weeks). All data presented are expressed as mean ± SE, unless stated otherwise for a specific value.Hypertension was produced by placing a silver clip with a 0.20-mm gap around the left renal artery; the contralateral kidney was left untouched. The rats were 10 weeks old at the time of constriction and average weight was 244 ± 11 g. All rats were housed...

Section: Discussionmentioning

confidence: 91%

Cardiac performance in rats with renal hypertension.

Averill

Ferrario

Tarazi³

et al. 1976

“…Thus, mitochondrial and myofibrillar masses respond to work overload differentially. Similarly, as hypertrophy proceeds, there is an increase in muscle mass and enlargement of individual muscle fibers (Geha et al, 1966); thereby, the cell surface-to-cell volume ratio may decrease as proposed for the hypertrophying dog heart (Wikman-Coffelt et al, 1975b), which thus may limit efficient exchange of metabolites and tissue gases.…”

Section: Progression Of Myocardial Hypertrophymentioning

confidence: 99%

The cardiac hypertrophy process. Analyses of factors determining pathological vs. physiological development.

Wikman‐Coffelt¹,

Parmley²,

Mason³

1979

265

COMPLICATED and even contradictory concepts concerning the biochemical and physiological aspects of cardiac hypertrophy are less enigmatic if we first discern whether the type of hypertrophy analyzed is physiological or pathological; i.e., whether factors secondary to the process of hypertrophy have induced the heart to augment or depress its mechanical function. In this review physiological hypertrophy is defined as hypertrophy accompanied by a normal or augmented contractile state in which the maximum rate at which myosin hydrolyzes ATP and the maximum velocity of muscle shortening are either normal or elevated. Pathological hypertrophy, on the other hand, is associated with depressed contractility without necessarily concordant heart failure, in which case the rate of myosin ATPase activity and the velocity of muscle shortening are decreased. Both types of hypertrophy may be considered compensatory in that the heart biochemically and physiologically adjusts to cellular alterations that occur according to the severity of the workload. Thus, our definition is not the same as that provided by Meerson (1976), since he did not distinguish between the two types of hypertrophy described here.To understand better the evolution of the cardiac hypertrophy process into physiological or pathological hypertrophy, this review is concerned with the immediate inciting stimuli of cardiac hypertrophy, the mechanism of its development, the various stages in its development, and its regional localization. We also are concerned with the dependency of

“…16 -^ Nevertheless, no consensus is currently available when considering only pressure-induced cardiac enlargement. Normal, 31 -^ depressed,' 3 -l4 and enhanced 33 -M heart function has been reported, but many different experimental animal species, forms, and durations of pressure overload and methods of functional evaluation are represented. Failure to recognize that several discrete biochemical phases occur during the myocardial response to pressure overload* 8 and/or that time-dependent hemodynamic fluctuations' 2 take place following aortic constriction undoubtedly contributes to the lack of consensus.…”

Section: -U -"mentioning

confidence: 99%

Pressure-induced cardiac enlargement in neonatal and adult rats. Left ventricular functional characteristics and evidence of cardiac muscle cell proliferation in the neonate.

Dowell¹,

McManus²

1978

SUMMARY Pressure-induced cardiac enlargement was created in neonatal (21 days of age) and adult (250-275 g) rats by abdominal aortic constriction. Sham-operated and aorta-constricted neonates were studied 2, 3, 4, and 5 weeks after surgery. Left ventricular weight was elevated by approximately 50% at all times studied. Radioautography demonstrated a marked elevation in 3 H-thymidine-labeled nuclei in cardiac muscle and nonmusde cells in aortaconstricted neonates. Other experiments examined the functional characteristics of hearts subjected to pressure overload while in either the neonatal or the adult state. Five weeks after surgery, left ventricular pressure and left ventricular weight were elevated to nearly identical degrees in both groups of experimental rat*. Under control conditions, heart rate and the maximum rate of left ventricular pressure development were not altered significantly in either neonatal or adult rats with aortic constriction. Aortic peak flow velocity, cardiac index, and stroke index also were within normal limits in neonates with aortic constriction; however, these measurements were reduced significantly in adults with aortic constriction. Stroke volume augmentation in response to saline infusion and inotropic responsiveness to isoproterenol were unaltered in aorta-constricted neonates but were markedly attenuated in aorta-constricted adults. The maintenance of normal heart functional characteristics represents a major point of distinction between pressure-induced cardiac enlargement in neonatal and aduh rats which correlates with the presence or absence of cardiac muscle ceD proliferation during adaptive heart growth.