Effect of rat hypophysectomy and growth hormone treatment on cardiac polysomes and ribonucleic acid

Earl, D.C.N.; Körner, A.

doi:10.1016/0003-9861(66)90062-2

Cited by 24 publications

(6 citation statements)

References 7 publications

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“…By elucidating rate-limiting factors in cardiac protein synthesis under different experimental conditions, insight may be gained into control mechanisms of protein synthesis, Previous investigations in vitro and in vivo indicate that cardiac protein synthesis is regulated by several factors, including hormones. Important hormones for regulation of heart protein synthesis are thyroxine (Scow 1959, Cohen et al 1966, Cohen and Whitbeck 1969, growth hormone (Earl and Korner 1966, AhrCn et al 1969, Hjalmarson et al 1970) and insulin (Wool 1965. Other important factors are: the supply of substrates (Rannels et al 1970), adequate oxygenation , amino acid supply and the mechanical activity of the tissue (Schreiber et al 1966, Kako andMinelli 1969).…”

Section: Discussionmentioning

confidence: 99%

In Vitro Work Load and Rat Heart Metabolism

Hjalmarson

Isaksson

1972

Acta Physiologica Scandinavica

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The isolated working rat heart preparation was used to study the effects of well defined work loads on heart protein synthesis. The rate of protein synthesis was evaluated by measuring the incorporation rate of phenylalanine‐3H into whole heart protein. Increased pressure load (afterload) accelerated the protein synthesis. A stimulatory effect was demonstrated with glucose or palmitate as substrate and with 1 or 5 times the normal rat plasma levels of all amino acids in the perfusion medium. The protein synthesis of both control and overloaded hearts was significantly accelerated with palmitate as substrate or with high levels of all amino acids. The work load effect could, thus, be obtained under conditions optimal for heart protein synthesis in vitro. In contrast to the stimulatory effect of in‐creased afterload the rate of protein synthesis was not changed when the left atrial filling pressure (preload) was increased, although the external heart work was raised several times. End systolic volume was markedly increased in pressure overloaded hearts compared to hearts perfused under control conditions or with increased preload. It is concluded that an increase in contractile tension during systole and/or an increase in the end systolic volume was a necessary requirement for the acceleration of protein synthesis.

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Section: Discussionmentioning

confidence: 99%

In Vitro Work Load and Rat Heart Metabolism

Hjalmarson

Isaksson

1972

Acta Physiologica Scandinavica

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“…A hepatoma with four times as much messenger RNA as rat liver was found to have far fewer polysomes than liver and more monomeric and dimeric ribosomes (Mansbridge & Korner, 1966). Changes in the ability of rat heart to incorporate amino acids into protein as a result of actinomycin treatment or hypophysectomy were not related to the proportion of the ribosomes which exist as polysomes (Earl & Korner, 1966).…”

Section: Does Growth Hormone Act By Directly Stimulating Messenger-rnmentioning

confidence: 90%

ANABOLIC ACTION OF GROWTH HORMONE^*

Körner

1968

Annals of the New York Academy of Sciences

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“…There was a significant correlation between the duration of acromegaly and cardiac abnormality. Thus, although the present GH levels were not shown to be correlated with the degree of cardiac hypertrophy (25) but with the duration of acromegaly, it is possible that prolonged hypersecretion of growth hormone is necessary for the development of cardiac abnormality (21). Recently we studied a group of patients with acromegaly (26) who had abnormal echocardiographic findings and enlarged hand volumes.…”

Section: Discussionmentioning

confidence: 93%

“…Thus, the results of this study may be explained by a direct effect of GH itself on the lung. In vitro and in vivo studies (20)(21)(22)(23)(24) have demonstrated the effect of GH on normal lung growth and the effect of excessive GH on the synthesis of collagen and especially mucopolysaccharides in soft tissues in the myocardium and probably in the lung. It was shown in a recent .…”

Section: Discussionmentioning

confidence: 99%

Hypoxemia and Pulmonary Function in Acromegaly^1,²

Luboshitzky¹,

Barzilai²

1980

Am Rev Respir Dis

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Pulmonary function was assessed in 11 patients with acromegaly, 8 of whom were previously treated by external pituitary irradiation. None of the patients had any overt respiratory ailment. Ventilatory function tests were normal in all patients and all had normal total lung capacity ranging from 75 to 123% (mean, 98.18 +/- 4.69%). Eight of ten patients (80%) had hypoxemia with a partial pressure of oxygen in arterial blood ranging between 58 and 90 mmHg (mean, 76.0 +/- 4.2). Calculated alveolar-arterial differences for oxygen ranged between 5.25 and 46.0 (mean, 26.0 +/- 4.7). In 4 of 5 patients in whom lung perfusion scans were performed, perfusion defects were found. There was a significant correlations (p < 0.05) between the presence of hypoxemia and the known duration of acromegaly, but not with the present growth hormone levels or previous therapy. The results indicate that pneumomegaly is not common in acromegaly. However, most patients have some degree of hypoxemia present usually as subclinical disease and it is probably due to a ventilation-perfusion derangement, which is probably a direct effect of the prolonged oversecretion of growth hormone.

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Effect of rat hypophysectomy and growth hormone treatment on cardiac polysomes and ribonucleic acid

Cited by 24 publications

References 7 publications

In Vitro Work Load and Rat Heart Metabolism

In Vitro Work Load and Rat Heart Metabolism

ANABOLIC ACTION OF GROWTH HORMONE^*

Hypoxemia and Pulmonary Function in Acromegaly^1,²

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Effect of rat hypophysectomy and growth hormone treatment on cardiac polysomes and ribonucleic acid

Cited by 24 publications

References 7 publications

In Vitro Work Load and Rat Heart Metabolism

In Vitro Work Load and Rat Heart Metabolism

ANABOLIC ACTION OF GROWTH HORMONE*

Hypoxemia and Pulmonary Function in Acromegaly1,2

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Product

Resources

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ANABOLIC ACTION OF GROWTH HORMONE^*

Hypoxemia and Pulmonary Function in Acromegaly^1,²