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B Chevalier

Publications and source records attributed to B Chevalier.

At least 91 records · Page 5Linked to original sources

Beta adrenergic and muscarinic receptors in compensatory cardiac hypertrophy of the adult rat.

The beta adrenergic (beta AR) and muscarinic (MR) receptors have been quantitated in parallel, using 125I-pindolol and 3H-quinuclidinylbenzilate, in a model of compensatory left ventricular (LV) hypertrophy (LVH), which developed in rats 4-6 weeks after an abdominal aortic stenosis. Since aortic banding resulted in a pronounced LVH of 62%, the results were expressed both in terms of density (fmol/mg protein) and quantity (fmol per LV). In addition, competition curves using either a specific beta 1-antagonist or isoproterenol or carbachol allowed the determination of the two beta AR subtypes and of the low and high affinity sites (defined by the inhibitory constant Ki) for both beta 1AR and MR. In LVH, receptor density decreased for each of total beta AR, beta 1AR subtype, high affinity (Ki 6-8 nM) beta 1AR sites (from 26 +/- 2 to 19 +/- 3 fmol/mg protein, P < 0.05), total MR and high affinity (Ki 12 nM) MR sites (from 63 +/- 6 to 40 +/- 4 fmol/mg protein, P < 0.001). The beta AR and MR densities dropped in parallel so that the MR/beta AR ratio remained unchanged. In sharp contrast (because the LVs were bigger) the quantities of total beta AR, beta 1AR subtype, beta 1AR high affinity sites, total MR and MR high affinity sites per LV were unmodified.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗

Arrhythmogenicity of the hypertrophied and senescent heart and relationship to membrane proteins involved in the altered calcium handling.

The high incidence of arrhythmias in human left ventricular hypertrophy has been well established but the mechanisms of arrhythmias are not well defined. In attempt to clarify these mechanisms, we tried to determine if a relationship might exist in the hypertrophied or senescent hearts between the incidence of arrhythmias and alterations in the gene expression of the main membrane proteins involved in the regulation of calcium movements. Holter monitoring was used in young and senescent rats where hypertrophy had been induced by aortic stenosis and hyperthyroidism (young rats) or by DOCA-salt treatment (senescent rats). Different types of spontaneous arrhythmias were detected. In the aortic stenosis group, the heart rate and the number of supraventricular premature beats were increased significantly, whereas the number of ventricular premature beats was increased in some animals but not in all. In senescent rats, the numbers of ventricular and supraventricular premature beats and the incidence of atrioventricular block were very high. At the cellular level, the density of calcium channels from the sarcolemma and of the alpha 1 subunit of the Na+/K(+)-ATPase were unchanged in the hypertrophied and senescent hearts but most of the proteins involved in the regulation of calcium movements (calcium release channel and Ca(2+)-ATPase from the sarcoplasmic reticulum, Na+/Ca2+ exchange, and beta adrenergic and muscarinic receptors from the sarcolemma) have a decreased density or activity. These changes might account for the slowing of the maximum shortening velocity and the impaired contractility of the hypertrophied and senescent hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

Beta 1 adrenergic receptor and G alpha s mRNAs in rat heart as a function of mechanical load and thyroxine intoxication.

OBJECTIVE: The aim of this study was to determine the expression of genes coding for the beta 1 adrenergic receptor and the alpha subunit of Gs in the adult rat normal and hypertrophied left ventricle, and in the left ventricle of the hypophysectomised rat after T4 intoxication. METHODS: Total RNA was extracted from normal, control, or hypertrophied left ventricles 5 weeks after aortic stenosis, and from left ventricles of control or T4 injected hypophysectomised animals. The expression of beta 1 adrenergic receptor and G alpha s mRNAs was quantitated by northern blot analysis and hybridisation with specific 32P-dCTP labelled DNA probes. RESULTS: beta 1 Adrenergic receptor mRNA was decreased (by 33%) in compensated left ventricular hypertrophy without modification of the relative level of G alpha s mRNA. The relative level of beta 1 adrenergic receptor mRNA correlated negatively with the degree of left ventricular hypertrophy, suggesting that the expression of the beta 1 adrenergic receptor gene is not activated by pressure overload. In the left ventricle of the hypophysectomised rat, a rapid increase in beta 1 adrenergic receptor mRNA (by 180% 3 h after hormone injection) was observed in response to T4, with no change in the relative content of G alpha s mRNA. These results provide evidence that beta 1 adrenergic receptor mRNA and G alpha s mRNA accumulate to different levels of abundance in the adult left ventricle, as indicated by their ratios (0.053 and 0.043 in sham operated and hypertrophied left ventricles respectively). This suggests that distinct mechanisms are involved in the control of the accumulation of these two mRNAs in cardiac tissue. CONCLUSIONS: The reduction in beta 1 adrenergic receptor density in the hypertrophied rat left ventricle is associated with a parallel reduction in the level of beta 1 adrenergic receptor mRNA. The beta 1 adrenergic receptor gene may belong to a group of genes which are not activated by pressure overload, but are responsive to thyroid hormone.

Animals↗

Triiodothyronine therapy in open-heart surgery: from hope to disappointment.

A controversy persists as to whether cardiopulmonary bypass (CPB) decreases plasma levels of triiodothyronine (T3), thereby justifying peri-operative administration of T3 to improve haemodynamic recovery. To examine the effects of T3 therapy on post-CPB haemodynamics and to determine whether the potential inotropic effects of T3 are mediated by an increase in beta-adrenergic responsiveness, a prospective, randomized, double-blind, placebo-controlled study was performed in 20 patients undergoing cardiac surgery with CPB. T3 or placebo solution (10 patients in each group) was given intravenously at the time of aortic unclamping and 4, 8, 12 and 20 h thereafter. End points included (1) thyroid hormone levels measured by radioimmunoassay (2) standard haemodynamic parameters (3) the density of lymphocyte beta-adrenoceptors measured by a radioligand (125I-iodocyanopindolol) binding technique. Post-CPB values (cross clamp removal) of T3 (pg.ml-1) were not significantly decreased compared with pre-CPB values: 3.3 +/- 0.2 vs 3.1 +/- 0.2 in controls and 3.3 +/- 0.4 vs 3.7 +/- 0.6 in T3-treated patients, respectively. The haemodynamic parameters were no different between the two groups at any postoperative time point. Likewise, density and affinity of lymphocyte beta-adrenoceptors were not significantly different from pre-operative values in either group. Thus, there seems to be no sound justification for a routine use of T3 in patients undergoing open-heart procedures.

Adult↗

Insulin-like growth factor-I-stimulated glucose transport in myotubes derived from chicken muscle satellite cells.

The effects of insulin and insulin-like growth factor-I (IGF-I) on glucose transport were compared in myotubes derived from chicken breast muscle satellite cells in vitro. Myotubes were incubated (for 0.5 or 4 h) with or without glucose in the presence or absence of insulin or IGF-I. Glucose uptake was subsequently measured by the incorporation of 2-[1,2-3H(N)] deoxy-D-glucose ([3H]2DG) in glucose-free medium (10 min at 20 degrees C). Glucose uptake was almost completely abolished by the addition of cytochalasin B or phloretin. It was increased by a decrease in glucose concentration in the incubation medium. Insulin (5 mg/l) stimulated [3H]2DG uptake to a maximum of 43 +/- 10% above basal after 30-min incubation and 101 +/- 15% after 4-h incubation. IGF-I and insulin at equimolar concentrations (25 micrograms/l and 20 micrograms/l respectively) were almost equipotent after 0.5 h but after 4-h incubation IGF-I was 17-fold more potent, suggesting that this 'late' effect was mediated through the IGF-I receptor. Incubation with cycloheximide suggested that the effect of IGF-I involved increased protein synthesis. The results suggest that chicken myotubes express a glucose transporter which is regulated by IGF-I and glucose concentration. However, they do not appear to express a typical insulin-responsive transport system.

Animals↗

Cardiac hypertrophy and failure--a disease of adaptation. Modifications in membrane proteins provide a molecular basis for arrhythmogenicity.

Cardiac hypertrophy is the physiological adaptation of the heart to chronic mechanical overload. Cardiac failure indicates the limits of the process. Cardiac hypertrophy is only one example of biological adaptation and results from the induction of several changes in gene expression, mostly of the fetal type, including those coding for the myosin heavy chain or the alpha-subunit of the Na+,K(+)-ATPase. From a thermodynamic point of view, the decrease in Vmax allows the heart to produce a normal tension at a lower cost. This process results from changes both in the sarcomere and in the expression of certain membrane proteins. The decrease in calcium transient is determined by several changes in membrane proteins that result in a rather fragile equilibrium in terms of calcium homeostasis. Any abnormal input in calcium will have exaggerated detrimental consequences on a hypertrophied myocyte and may cause automaticity and arrhythmias or an exaggerated response to anoxia in terms of compliance.

Adaptation, Physiological↗

The membrane proteins of the overloaded and senescent heart.

Cardiac hypertrophy which occurs during chronic mechanical overload is one of the numerous examples of biological adaptation to environmental requirements. As such, it is obtained at random by trial and error, and adaptation represents the sum of various modifications in gene expression, including the shift in isoform of myosin or in iso Na+, K+ ATPase, the decrease in beta-adrenergic and muscarinic receptors, ryanodine channels or SR Ca2+ ATPase densities and the unchanged density in Ca2+ current. Some of these changes are beneficial at the cellular level, but are finally detrimental for the organism as a whole, as is the slowing of Vmax. It was suggested that the calcium homeostasis of the hypertrophied cardiocyte was fragile and that this modified cell was less able to buffer the changes in the intracellular calcium, thus providing a biological basis for the arrhythmogenicity of the hypertrophied heart. These various modifications may provide a new key for future pharmaceutical research.

Adaptation, Physiological↗

Remodeling of the heart (membrane proteins and collagen) in hypertensive cardiopathy.

The basis for impaired left ventricular function of hearts in moderate to severe stages of hypertrophy and congestive heart failure remains uncertain. At the cellular level, the mechanisms governing the movements of calcium in the myocardium are actually depressed and might at least in part account for the slowing of the maximum shortening velocity and the impaired relaxation. These alterations of membrane proteins seem particularly important in species where the slowing of Vmax cannot be a consequence of the myosin heavy chain shift. They lead to an unstable equilibrium of calcium homeostasis and to calcium overload in heart failure. On the other hand, the enhanced density and remodeling of collagen in the hypertrophied heart, which would depend on elevation in circulating aldosterone, impair myocardial stiffness with diastolic dysfunction and lead to altered pumping capacity of the heart. Disturbances of calcium metabolism and matrix collagen remodeling enhance early afterdepolarizations and arrhythmias.

Animals↗

[Rapid diagnosis of malaria. The microwave furnace].

Thick blood is a well known method for malaria diagnosis, very faithful and sensitive, but it could not be used in emergency because it had to dry for many hours. Micro-wave over allows a quick drying (two minutes). Do it can now be used in emergency.

Animals↗

Alterations in beta adrenergic and muscarinic receptors in aged rat heart. Effects of chronic administration of propranolol and atropine.

The cardiac responses to sympathetic and vagal stimulations are attenuated with ageing. To understand these findings, the densities of beta adrenergic (beta R) and muscarinic (MR) receptors in the left ventricles have been quantitated in parallel in male Wistar rats (4- and 24-month-old) using [125I]iodocyanopindolol and [3H]quinuclidinyl benzilate as specific radioligands. The homologous regulation of these receptor densities was also explored after a 7-day continuous infusion of propranolol or atropine. As compared to young rats, the beta R and MR densities in aged animals were decreased (from 31 +/- 2 to 23 +/- 2 fmol/mg protein, P less than 0.05 for beta R; from 104 +/- 7 to 54 +/- 3 fmol/mg protein, P less than 0.001 for MR) but the diminution in MR was more pronounced (-48%) than that in beta R (-26%), resulting in a drop in the beta R/MR ratio. Continuous infusion of propranolol or atropine up-regulated the beta R and MR densities (respectively +50%, P less than 0.01 and +33%, P less than 0.05) in aged but not in young adult rats. We therefore conclude: (i) that the diminution of the cardiac response to the sympathetic and vagal stimulations during ageing may be partly explained by a decrease in the corresponding receptor density; (ii) these changes are reversible and the density of these two groups of receptors can return to adult control values by chronic administration of the appropriate antagonist.

Aging↗

Normal number and kinase activity of insulin receptors in liver of genetically fat chickens.

Genetically fat (FL) chickens exhibit an increase in liver lipogenesis and, in the fasting state, insulin sensitivity compared with genetically lean (LL) chickens. Liver insulin receptor number and insulin receptor kinase (IRK) activity were studied at 5 wk. In the fasting (16 h) and fed state, insulin binding to liver membranes and insulin receptor affinity (50% inhibition of tracer binding, range: 5-7 ng/mL at 4 degrees C) were very similar in fat and lean chickens. Insulin degrading activity of membranes was negligible for both genotypes. Following solubilization with Triton X-100, liver receptors were purified either on wheat germ agglutinin (WGA receptors) or on lentil then wheat germ lectins (lentil receptors). Both types of purified receptors exhibited the same binding affinity, independent of the genotype or the nutritional state. Autophosphorylation and IRK activity toward artificial substrate poly(Glu, Tyr)4:1 were not different between genotypes. Basal IRK (i.e., in the absence of insulin) was decreased by the overnight fast. Fattening of genetically fat chickens cannot be accounted for by an increase in the number or the kinase activity of liver insulin receptors. Steps following the binding or the receptor kinase may be involved.

Animals↗

Insulin sensitivity and liver insulin receptor structure in ducks from two genera.

Insulin sensitivity and liver insulin receptor structure were studied in 5-wk-old ducks from two genera (Muscovy and Pekin). In the fasting state, both duck types were equally resistant to exogenous insulin compared with chicken. Despite the low potency of duck insulin, the number of insulin receptors was lower in Muscovy duck and similar in Pekin duck and chicken liver membranes. After 125I-insulin cross-linking, the size of the alpha-subunit of the receptors from the three species was 135,000. Wheat germ agglutinin-purified receptors from the three species were contaminated by an active and unusual adenosinetriphosphatase (ATPase) contaminant (highest activity in Muscovy duck). Sequential purification of solubilized receptor from both duck types on lentil and then wheat germ agglutinin lectins led to a fraction of receptors very poor in ATPase activity that exhibited a beta-subunit size (95,000) and tyrosine kinase activity similar to those of ATPase-free chicken insulin receptors. Therefore the ducks from the two genera exhibit an alpha-beta-structure for liver insulin receptors and a clear difference in the number of liver insulin receptors. Their sensitivity to insulin is, however, similarly decreased compared with chicken.

Animals↗

Membrane proteins of the myocytes in cardiac overload.

Hypertrophy of the cardiac myocytes resulting from a mechanical overload may be responsible for major membraneous modifications, either at a sarcolemmal or at a sarcoplasmic level. In the present report, evaluation of several sarcolemmal markers such as beta-receptors, muscarinic receptors or (Na+,K+)-ATPase has been realized on an experimental model of cardiac hypertrophy performed on adult rats. Special attention has been taken to compare results expressed in densities or expressed in number of receptors present at the cellular level. For example, the beta-receptors density was 30% decreased whereas calculations of number of receptors present in the myocytes revealed an unchanged number (around 20,000 in both groups). The unmodified number could suggest a non regulation for the genes coding for the receptors.

Animals↗

[Retrograde dissection of the common trunk of the left coronary vessel during angioplasty of left anterior descending coronary artery. Apropos of 2 cases].

Acute dissection of the left main coronary artery during coronary angiography or angioplasty is a rare but well known complication; it is attributed to a mechanical trauma caused by the tip of the catheter guide wire. The authors present two cases of dissection at the site of coronary angioplasty with a retrograde extension to the left main stem requiring emergency coronary surgery.

Aged↗

[Hemodynamic response to intracoronary injection of a vasodilator during coronary angiography. A randomized comparative study of trinitrin and linsidomin ].

Intracoronary injection of a vasodilator agent in an almost systematic practice during coronary angiography or angioplasty because of the dynamic information that it provides concerning the stenosis, the artery in the unstenosed segment and spastic phenomena. Nitroglycerin is the reference drug with, however, a significant dose-dependent hypotensive effect. The aim of this randomised open trial was to compare the effects of Linsidomine, the active metabolite of molsidomide with the reference product. Eighty patients aged 59.2 +/- 10.4 years received either 0.15 mg of nitroglycerin or 0.8 mg of linsidomine during coronary angiography. Aortic pressure and heart rate were monitored continuously over 3 minutes; at the 3rd minute and injection of contrast was performed under fluoroscopic control under the same conditions as the basal injection for an experienced coronary angiographist to judge semi-quantitatively the quality of vasodilation at the site of stenosis and in the whole artery. In the linsidomine group, the only significant change was a moderate fall in systolic pressure from the 1st to the 3rd minute. In the nitroglycerin group, all pressure parameters fell from the 30th second. The heart rate remained stable in both groups. The maximal pressure differences were significantly different in the two groups: -4 +/- 7.3 mmHg versus -11.3 +/- 9.2 mmHg (linsidomine versus nitroglycerin), p less than 0.001 for systolic pressure; -0.1 +/- 5 mmHg versus -3 +/- 5.4 mmHg respectively for diastolic pressure (p less than 0.05); and -1 +/- 6 mmHg versus -5.3 +/- 6.4 mmHg (p less than 0.01) for mean pressure. These pressure changes were not associated with any detectable untoward clinical effect in either group of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

[Transesophageal echography in the investigation of left atrial ball thrombi. Apropos of a case of migration of a left atrial thrombus].

The authors report the case of a pediculated left atrial ball thrombus whose embolisation and ejection through the aortic valve was recorded during transesophageal echocardiography. The value and risks of transesophageal echocardiography for the diagnosis of left atrial masses are reviewed in the light of this case and a review of the literature. The prognosis and therapeutic implications of a left atrial ball thrombus are also described.

Aged↗

Membrane proteins of the myocytes in cardiac overload.

1. Hypertrophy of the cardiac myocytes resulting from a mechanical overload may be responsible for major membraneous modifications, either at the sarcolemmal or at the sarcoplasmic level. In this study several sarcolemmal markers such as beta-adrenoceptors, muscarinic receptors or (Na+, K+)-ATPase were investigated in an experimental model of cardiac hypertrophy, the chronic aortic stenosis in adult rats. 2. Left ventricular beta-adrenoceptor density (expressed in fmol mg-1 protein) was decreased in the aortic stenosis group by about 30%; however, when expressed in number of receptors per cardiac cell beta-adrenoceptor number in the hypertrophied myocytes was unchanged. 3. Similarly, the number of muscarinic receptors in the hypertrophied cells, expressed as number of receptors per cardiac cell, was unchanged. 4. The number of (Na+, K+)-ATPase molecules with high affinity for ouabain was markedly increased in the hypertrophied myocytes, while those with low affinity for ouabain were not. 5. These results indicate the necessity in chronic hypertrophy to calculate receptors not only in density (fmol mg-1 protein) but also in number per cardiac cell. The unchanged number of beta-adrenergic and muscarinic receptors present on the hypertrophied myocytes suggests a non-regulation for the genes coding for these receptors.

Animals↗

Impaired insulin action but normal insulin receptor activity in diabetic rat liver: effect of vanadate.

In vivo insulin resistance is a characteristic of the liver and peripheral tissues in 10-wk-old female rats with non-insulin-dependent diabetes induced by streptozotocin given on day 5 after birth. Oral administration of vanadate (0.2 mg/ml) for 20 days in the diabetic rats lowered their plasma glucose levels to normal values without affecting their basal plasma insulin levels. In the basal state as well as after submaximal or maximal hyperinsulinemia (euglycemic clamp studies), peripheral glucose utilization and hepatic glucose production in vivo were normalized in the diabetic rats after the vanadate treatment. In wheat germ agglutinin purified receptors, 125I-labeled porcine insulin binding, basal and insulin-stimulated insulin receptor kinase activities for both the autophosphorylation of the beta-subunit and the phosphorylation of the artificial substrate poly (Glu-Tyr) 4:1, were found identical in diabetic and control rats, treated or not with vanadate. Liver phosphoenolpyruvate carboxykinase activity was significantly enhanced in untreated diabetic rats (P less than 0.01) as compared with control rats and returned to normal values after the 20-day vanadate treatment. Thus, in that model of non-insulin-dependent diabetes, 1) oral vanadate exerts a corrective insulin-like effect on impaired insulin action both at the level of liver and peripheral tissues, 2) impaired insulin action with no alteration of the insulin receptor tyrosine kinase is observed in the liver of untreated rats, and 3) corrective effect of vanadate on liver glucose metabolism is probably distal to the insulin receptor kinase activity.

Animals↗