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Biomedical subjects

H E Morgan

Publications and source records attributed to H E Morgan.

At least 91 records · Page 5Linked to original sources
PubMed1978

Effect of insulin on kinetics of sugar transport in heart muscle.

Insulin increased the maximal rate of sugar transport in the perfused rat heart, but had essentially no effect on the Michaelis constant of sugar entry or half-maximal constant for equilibrium exchange. In control hearts, the following kinetic parameters of 3-O-methylglucose transport were measured: Michaelis constant for entry, 7-10 mM; equilibrium exchange constant, 7 mM; and activity constant (Vmax/Km) from 0.02 to 0.1 ml/g.min. In insulin-treated hearts, these values were 6 mM, 3 MM, and 2.2 ml/g.min, respectively. These changes in transport constants were consistent with a model in which 1) sequestered carrier was released by the hormone or 2) carrier movement, in all forms and directions, was accelerated. Measurements of glucose transport in control hearts indicated that the Michaelis constant for entry was 4 mM and the activity constant, 0.5 ml/g.min. In insulin-treated hearts, quantitation of transport parameters was prevented by accumulation of intracellular glucose.

Animals↗
PubMed1978

Hormonal and metabolic control of proteolysis.

Proteolysis in heart muscle is regulated by hormonal and metabolic factors. In the absence of insulin, protein degradation accelerated, autophagic vacuoles appeared within the heart and latency of lysosomal enzymes decreased. Addition of insulin prevented or reversed these changes. Provision of leucine inhibited proteolysis in control hearts. Addition of the products of transamination and oxidative decarboxylation of leucine, isoleucine and valine had similar inhibitory effects. Protein degradation was inhibited in ischaemic or anoxic hearts, but latency of lysosomal enzymes was decreased. Inhibition of degradation in energy-poor tissue may represent both an energy-requirement for proteolysis and inhibition by accumulation of metabolic products, such as lactate.

Adenosylmethionine Decarboxylase↗
PubMed1976

Effects of anoxia and ischemia on protein synthesis in perfused rat hearts.

The effect of ischemia on synthesis of myocardial proteins was investigated using a model of perfusion in which low levels of coronary flow were provided to paced hearts worked against a closed aortic outflow tract. These conditions rapidly produced ischemia and ventricular failure, as evidence by reduced coronary flow, increased left atrial pressure, and decreased pressure development. Protein synthesis was inhibited in a subsequent 1-hour period, during which a minimal coronary flow was maintained by retrograde perfusion. ATP, GTP, and creatinine phosphate were depleted in ischemic hearts and AMP accumulated. Production and accumulation of lactate within the tissue increased, whereas palmitate uptake was inhibited. The inhibition of protein synthesis was not associated with reduced levels of intracellular amino acids. During ischemia, decreased levels of ribosomal subunits as compared to paced or unpaced aerobic hearts suggested that peptide chain elongation was slow relative to initiation. Provision of insulin further reduced subunit levels but did not increase protein synthesis, suggesting that the hormone did not prevent inhibition of peptide chain elongation in energy-poor hearts.

Aerobiosis↗
PubMed1975

Effects of hypophysectomy, growth hormone, and thyroxine on protein turnover in heart.

Cardiac atrophy following hypophysectomy was accompanied by decreased heart content of RNA and polysomes and increased levels of ribosomal subunits, suggesting that protein synthesis was restricted by a reduced supply of ribosomes and an imbalance between rates of peptide-chain initiation and elongation. During perfusion in vitro, provision of palmitate restored the normal balance between rates of initiation and elongation but protein synthesis was lower in hearts of hypophysectomized than normal rats, reflecting the lower RNA content of hearts from hormone-deficient animals. After the period of atrophy had passed, or after treatment with growth hormone and thyroxine, heart RNA content and rates of protein synthesis were equal to or greater than those found in normal hearts. When plasma levels of amino acids, glucose, fatty acids, and insulin, and rates of beating and ventricular pressure development observed in normal and hypophysectomized rats were simulated during in vitro perfusion, hearts from hormone-deficient rats had reduced rates of protein synthesis but unaltered rates of degradation. Cathepsin D activity in heart homogenates (+ Triton X-100) was elevated during cardiac atrophy when expressed per g of tissue but not when expressed per heart.

Acetylglucosamine↗
PubMed1975

Effect of insulin on protein turnover in heart muscle.

The effect of insulin on turnover of protein was investigated in isolated perfused rat hearts. The hormone lowered intracellular levels of nine amino acids and reduced or abolished net release of 10 amino acids and ammonia. The extent of the insulin effect on protein degradation was investigated by estimating the rate of dilution of the specific radioactivity of the free phenylalanine pool. Insulin concentrations greater than 200 microunits per ml reduced protein degradation and net phenlylalanine release. Protein degradation was estimated more directly by inhibiting reincorporation of nonradioactive phenylalanine from protein with cycloheximide. Addition of the inhibitor increased the estimated rates about 50%, but the magnitude of the hormone effect was similar. The latency of lysosomal enzymes in control and insulin-treated hearts was assessed by measuring activities of beta-acetylglucosaminidase and cathepsin D in heart homogenates in the presence and absence of Triton X-100. Perfusion with insulin-free buffer increased the activities assayable without detergent, but did not change total activities of these enzymes. Insulin decreased activities assayable without detergent and increased activities sedimenting in the 10-5 times g pellet. These studies showed that insulin restricted the rate of protein degradation in the isolated perfused rat heart. Concomitantly, the latency of lysosomal enzymes was increased when the hormone was provided.

Adenosine Triphosphate↗
PubMed1975

Isolated heart perfusion techniques for rapid screening of myocardial preservation methods. Anoxia versus ischemia.

Isolated nonworking and working heart preparations are described and recent modifications that increase their reliability and scope are reviewed. Isolated perfused tissues are superior to other models for screening myocardial preservation techniques. The metabolic and functional differences between anoxia and ischemia are stressed, myocardial glycolysis is reviewed, and from basic studies potentially fruitful avenues for investigation of myocardial preservation techniques are outlined. Better application of available knowledge of myocardial metabolism could further reduce the risks of cardiac operation.

Animals↗
PubMed1975

Bilateral adrenal enlargement in Addison's disease caused by tuberculosis. Nephrotomographic demonstration.

Nephrotomography showed markedly enlarged adrenal glands in a 67-year-old man with acute Addison's disease due to tuberculosis. Other causes of acute adrenal insufficiency associated with enlarged adrenals are histoplasmosis and, rarely, bilateral metastatic carcinoma, amyloidosis, or hemorrhage. Radiologic demonstration of large adrenal glands in a patient with acute Addision's disease should strongly suggest an infectious etiology.

Addison Disease↗