Studies on Myocardial Protein Metabolism in Cardiac Hypertrophy

Tomita, Kazuo

doi:10.1536/ihj.7.566

Cited by 18 publications

(3 citation statements)

References 3 publications

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“…Augmented protein synthesis has been regularly seen in the left ventricle accompanying elevated aortic pressure both in vitro (6,7,8,20) and in vivo (21,22,23), but it has been difficult to separate the protein synthesis-pressure relationship from changes in coronary perfusion (20), since afterload in the left ventricular models increases coronary flow during the application of the afterload. Increased protein synthesis has also been seen in the nonperfused papillary muscle stimulated with increased tension (24), although here passive stretch also showed some increase in synthesis.…”

Section: Progressive Right Ventricular Hypoxiamentioning

confidence: 99%

The effect of pressure or flow stress on right ventricular protein synthesis in the face of constant and restricted coronary perfusion.

Schreiber¹,

Rothschild²,

Evans³

et al. 1975

J. Clin. Invest.

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A B S T R A C T Cardiac stress produced by hypertension or excess volume loading results in different types of hypertrophy. Elevated left ventricular pressure rapidly results in increased myocardial protein synthesis in vivo and in vitro, but such rapid alterations are not consistently seen in volume loading. The difference in response is difficult to clarify since it is not possible to effect alterations in left ventricular pressure or perfusion without profoundly affecting coronary perfusion. The present study describes cardiac protein synthesis in the right ventricle of the young guinea pig heart in vitro by utilizing a perfusion model in which the right ventricle could be stressed by elevations of pressure or volume loading in the presence of constant and restricted coronary perfusion. With coronary flow maintained at 4 ml/min per heart equivalent to 25 ml/min/g dry wt, an increase in right ventricular pressure from normal levels of 3 mm Hg to 11 mm Hg resulted in a 60% increase of myocardial incorporation of [14C] INTRODUCTIONCardiac stress produced by experimental hypertension or excess volume loading eventually results in hypertrophy (1-3) though the mechanisms and types of hypertrophy may be different in each stress, e.g., concentric hypertrophy with little increase in ventricular volume is described in hypertension or valvular stenosis while hypertrophy with dilatation is most often seen in valvular insufficiency or volume stress (4, 5). Acute aortic hypertension or volume loading is also accompanied by increased coronary flow which has been shown to enhance protein synthesis (6-8), and few data are available on the effects of such loading in the face of controlled or restricted coronary perfusion.The present report presents data obtained with an in vitro perfusion modal which was designed to separate pressure and volume stresses in the right ventricle from alterations in coronary perfusion and which permits study of protein synthesis in this ventricle in the presence of controlled as well as restricted coronary flow. Two patterns are indicated with this model of the young guinea pig heart. First, protein synthesis is stimulated by acute pressure stress but not by acute volume loading. Second, with maximum stresses right ventricular protein synthesis returns to control levels. A preliminary description of this model was previously reported (9). METHODS Received for publication 8 October 1973 and in revised Young male guinea pigs, 260-320 g, approximately 4-6 wk form 16 September 1974.after weaning, were used in all the studies. The diet beforeThe Journal of Clinical Investigation Volume 55 January 1975 -1-11 1 the operation and anesthesia were as described previously (6, 7). After anesthesia, the chest cage was opened and the proximal aorta cannulated and perfused with oxygenated Krebs-Henseleit solution containing amino acids in concentrations previously described (6, 10). The pulmonary artery was then cannulated with a no. 240 nondistensible polyethylene catheter which was gently passed through the p...

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Section: Progressive Right Ventricular Hypoxiamentioning

confidence: 99%

The effect of pressure or flow stress on right ventricular protein synthesis in the face of constant and restricted coronary perfusion.

Schreiber¹,

Rothschild²,

Evans³

et al. 1975

J. Clin. Invest.

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“…Although some investigators have suggested that there is a stimulation of protein synthesis by increased volume workload in Vol. 216 vitro (Schreiber et al, 1966;Tomita, 1966), most investigators agree that there is no such effect (Hjalmarson & Isaksson, 1972a;Schreiber et al, 1975Schreiber et al, , 1981.…”

mentioning

confidence: 99%

Stimulation of left-atrial protein-synthesis rates by increased left-atrial filling pressures in the perfused working rat heart in vitro

Smith¹,

Sugden²

1983

Biochemical Journal

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We investigated the effect of an increase in the left-atrial filling pressure on the rate of left-atrial protein synthesis in the left-side-perfused working rat heart preparation of Taegtmeyer, Hems & Krebs [(1980) Biochem. J. 186, 701-7111. An increase in filling pressure (preload) at a constant aortic pressure (afterload) increased both the intra-atrial pressure and the atrial stroke volume. The aortic pressure (afterload) was held constant. An increase in filling pressure from 5 to 20cmH20 at an aortic pressure of 70cmH2O, or an increase in filling pressure of 7.5 to 20cmH20 at an aortic pressure of 100 cmH20, significantly stimulated the rates of left-at-rial protein synthesis by 30-40%. The stimulation was observed when the rates of protein synthesis were expressed relative to either protein or RNA content. Since perfusate entering the right atrium from the coronary circulation left that atrium passively, the rate of protein synthesis in this compartment can be used as an internal control. Rates of right-atrial protein synthesis were similar to those in the left atria exposed to the lower filling pressures and were unaffected by the increases in left-atrial filling pressure. We suggest that the acute effects of increased left-atrial filling pressure on protein synthesis in that compartment may be important in the development of left-atrial hypertrophy. This condition is seen in patients who have raised pulmonary venous pressures in, for example, mitral stenosis.

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“…The concentration of myofibrillar protein and its proportion of cellular volume increase gradually in the course of ventricular adaptation to chronic pressure overload [30,34,37]. Since the fractions of water and other non-protein material remain the same in Goldblatt rats [20], other components of the cell must be reduced [28].…”

Section: Discussionmentioning

confidence: 99%

Left ventricular enzyme activities of the energy-supplying metabolism in Goldblatt-II rats

Koehler

Medugorac

1985

Res. Exp. Med.

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The hypertrophied left ventricles of renovascular hypertensive Wistar rats were examined for several enzyme activities 4-6 and 8-12 weeks after operation (Goldblatt-II), and compared with controls. The activities of beta-hydroxyacyl-CoA dehydrogenase in hypertrophied myocardial tissue were found to be markedly diminished, as were those of citrate synthase, although to a lesser degree. In both stages of left ventricular hypertrophy hexokinase activity was considerably increased, whereas that of lactate dehydrogenase was only initially slightly elevated. Both enzymes showed an altered isoenzyme composition. The possible reasons and consequences of these changes are discussed.

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Studies on Myocardial Protein Metabolism in Cardiac Hypertrophy

Cited by 18 publications

References 3 publications

The effect of pressure or flow stress on right ventricular protein synthesis in the face of constant and restricted coronary perfusion.

The effect of pressure or flow stress on right ventricular protein synthesis in the face of constant and restricted coronary perfusion.

Stimulation of left-atrial protein-synthesis rates by increased left-atrial filling pressures in the perfused working rat heart in vitro

Left ventricular enzyme activities of the energy-supplying metabolism in Goldblatt-II rats

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