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Biomedical subjects

C Delcayre

Publications and source records attributed to C Delcayre.

45 records · Page 3Linked to original sources
PubMed1982

Biology of cardiac overload.

Mechanical overload in the heart induces two different types of adaptational mechanisms. (a) From a qualitative point of view, the maximum speed of shortening is depressed in relation to a myosin isoenzymic change responsible for decreased ATPase and, although the relaxation appears normal from a physiological point of view, the existence of an abnormality in Ca2+ uptake in the sarcoplasmic reticulum has been well documented. Both of these processes appear to improve efficiency by decreasing the heat produced per gram of tension. The existence of a large broadening of the action potential has now been well established, but it remains unexplained at the biochemical level. The functioning of mitochondria is rather controversial, and although it has been shown that they are both more abundant and smaller, the reason why their respiratory index changes remains unknown. (b) From a quantitative point of view, the adult heart adapts to overload by increasing its mass. This is mainly a consequence of a hypertrophy of the myocytes and a mitotic multiplication of nonmuscular cells. Data suggest that myocyte amitotic divisions may occur, at least in humans, and perhaps in very sizeable experimental hypertrophy. To this phenomenon has been added the development of polyploidy of myocyte nuclei, which seems to be specific to certain species. The stimulation of protein synthesis occurs very soon after pressure overload, and is delayed in volume overload; protein lysis also increases, although this is controversial. The process occurs whatever the proteins. This is accompanied by increased nuclear activity and a stimulation in RNA synthesis, which is especially precocious for messenger RNA. Among the very early events which could be potential signals for protein synthesis, attention has been focused on polyamine, RNA polymerase, and uridine kinase. The trigger mechanism, of course remains hypothetical. As a trigger for protein synthesis, several data suggest an increase in wall stress and stretch; a drop in efficiency is suggested as a trigger for qualitative changes.

Action Potentials↗
PubMed1979

Myosin synthesis and enzymatic properties during thyroxine intoxication in rabbits.

Hyperthyroidism has been induced to rabbits by a daily subcutaneous injection of D-L thyroxine (0.3 mg/kg). The ventricular myosin Ca2+ ATPase was increased after one week and reached + 100 % after two weeks while the K+ EDTA ATPase remained normal. During the same period, the heart weight, and the myosin incorporation of 3H-lysine after a four hour period of labelling had increased in parallel. The enhancement of both the Ca2+ ATPase and the labelling of myosin correlate, which suggests the appearance of a new molecule during the course of intoxication. This biochemical abnormality was unchanged after treatment with propranolol.

Animals↗
PubMed1975

A comparative study of heart myosin ATPase and light subunits from different species.

Heart myosin ATPase (measured with 10 mM CaCl2, and 0.60 M KCl) was found to be higher in rats (423 nmoles of Pi/min/mg) than in guinea-pig (268 nmoles of Pi/min/mg), dogs (139 nmoles of Pi/min/mg) or rabbits (94 nmoles of Pi/min/mg). Rat heart myosin ATPase was found to be higher than that from a pure red skeletal muscle myosin (soleus from guinea-pig: 286 nmoles/min/mg) and only one third lower than that from fast skeletal muscle myosin from rabbits. The heart myosin ATPase from rat, guinea-pig, and rabbit correlates with the maximum velocity of shortening at zero load of the myocardial muscle, as determined by other authors. These four cardiac muscle myosins have the same two light subunits (M.W.: 27000 and 18000) in SDS polyacrylamide gel electrophoresis; one of them (M.W.: 18000) exists in guinea-pig and dog as two different molecules having a different charge, as shown in urea electrophoresis, but in the rat, this subunit is also unique in urea gel electrophoresis. Rat heart, apparently, does not possess the phosphorylated light subunit (M.W.: 18,000) described by others in rabbit heart myosin. Attempts have been made to obtain a highly purified myosin, but this procedure does not suppress the striking difference which exists between rat and dog heart myosin ATPase.

Adenosine Triphosphatases↗
PubMedDate not supplied

Hormonal induction of c-fos and HSP68 mRNAs on an isolated coronary perfused adult rat heart.

Transient growth signals which can be related to protein synthesis and cellular growth are of particular interest in the heart because of the incidence of cardiac hypertrophy in man. The isolated coronary perfused adult rat heart or the so-called Langendorff preparation, is an useful model in exploring not only protein synthesis but also c-fos/c-myc protooncogene and Heat Shock Protein (HSP) gene expression. Phenylephrine infusion in this preparation induces c-fos expression whether the heart is beating or reversibly or irreversibly arrested by solutions enriched in KCl. Norepinephrine has the same effect. Quantitative analysis with slot blots shows that in both cases the adrenergic effect has a dual origin since it is inhibited both by propranolol, a beta-adrenergic antagonist, and terazosine, a soluble alpha 1-adrenergic antagonist. We conclude that the isolated heart is a useful tool to explore the early changes in gene expression which occur in this tissue in response to various physiological stimuli.

Animals↗
PubMedDate not supplied

Left ventricular compliance in the DOCA-salt model of hypertension in the rat. Effects of propranolol.

The aim of this study was to see if an enhanced myocardial stiffness is an inevitable consequence of the increase in cardiac mass and to analyze the effects of beta-adrenergic blockade on this parameter. The DOCA-salt model of hypertension was used to induce cardiac hypertrophy in the rat. After 6 weeks, the hearts of the DOCA-salt-treated animals were hypertrophied by 67%, and the left ventricular weight, the left ventricular/body weight ratio and the left/right ventricular weight ratio were similarly increased. Isolated hearts were retrogradely perfused at a constant flow of 15 ml/min/g tissue. Contractile parameters were recorded using an intraventricular balloon whose volume was manually adjusted. For each heart, a sequence of three systolic and diastolic pressure-volume curves were constructed: in Krebs alone, after addition of 10(-6) M of propranolol, and after KCl-arrest. In spite of a pronounced degree of hypertrophy, the DOCA-salt hearts had a normal diastolic pressure-volume curve and both the chamber and tissue stiffness constants were not modified. This result indicates that a depressed compliance does not necessarily accompany hypertrophy, especially in a DOCA-salt model in which the collagen content of the heart is unchanged. The systolic pressure-volume curve was greatly modified and shifted to the left indicating an enhanced capacity of the hypertrophied heart to generate force. This increase persisted even when the systolic pressure has been divided by the heart weight. beta-Blockade slightly depressed the contractility of the isolated heart at pharmacological concentrations. At high concentrations, cardiac dilatation was induced. This enhancement in ventricular distensibility had no consequences on diastolic compliance constants. It is thus concluded that, during cardiac hypertrophy, the changes in passive stiffness of the ventricle are more related to collagen content than to the cardiac mass and that beta-adrenergic blockade has no effect on the passive properties of the ventricle.

Animals↗
PubMedDate not supplied

[The cardiovascular steroid system].

In this review, the authors describe: (1) the different types of glucocorticoid hormone receptors, on the cell membrane and two types inside the cell, the MR and GR (mineralo- and glucoreceptors); (2) the synthesis of the hormones with the decisive role of the final enzymes, 11 beta-hydroxylase and aldosterone-synthetase; (3) the increasing evidence for a cardiovascular steroid system in the vessels as well as in the myocardium. The authors have reported new data suggesting the existence of an endocrine cardiac steroidogenic system in the heart with a potential physiological and pathological relevance (for transmembrane ion transport and trophic alterations).

Adrenal Cortex Hormones↗