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Biomedical subjects

P Chatelain

Publications and source records attributed to P Chatelain.

At least 217 records · Page 12Linked to original sources
PubMed1984

Histological diagnosis of myocardial infarction: the role of calcium.

The value of a histochemical method (alizarin red S) based on the detection of calcium in myocytes in early myocardial infarction was tested on 20 human and 30 rat hearts. After alizarin red S stain, a yellow-gold aspect of myocytes allowed to diagnose myocardial infarction in 18/20 human hearts, whereas with macroscopic examination and conventional histology the diagnosis was made only in 12/20 cases. In the rat, 30 min after coronary ligation, the ischaemic zone appeared yellow-gold with alizarin red S. This suggested that such a staining would also indicate an early infarct in human hearts. However, the yellow-gold aspect of myocytes with alizarin red S is unusual for calcium staining, which is generally orange. Consequently, the notion of calcium overload in 'yellow-gold' myocytes needed confirmation. This was done using a scanning electron microprobe quantometer (SEMQ), which showed a significantly high calcium level in the alizarin red S yellow-gold-stained myocytes. Our findings suggest that a single histochemical method for calcium (alizarin red S) is useful for detecting irreversible ischaemia and helps to diagnose very early myocardial infarction morphologically.

Animals↗
PubMed1984

Receptor binding profile of tibalosine, a new antihypertensive.

The ability of 1-(2,3-dihydro-5-benzo[b]thienyl]-2-(4-phenylbutylamino)-1- propanol-(erythro) (tibalosine, CP 804 S), a new antihypertensive agent, to interact with 11 different receptors has been studied by binding assays. Tibalosine interacts specifically with alpha- and beta-adrenergic receptors and calcium channel binding sites. Ki values (nmol/l) for inhibition of specific binding are 26, 1000, 1000 and 770 respectively for the alpha 1-adrenergic, beta 1- and beta 2-adrenergic receptors and calcium channel binding sites. The interaction with adrenergic receptors is stereoselective since CP 804 S/T, the threo derivative of tibalosine, exhibits Ki values 8 to 10 times higher than those of tibalosine. The selectivity ratio between alpha 1- and alpha 2-adrenergic receptors is about 400. Tibalosine and CP 804 S/T interact with the low affinity binding sites labelled by 3H-WB 4101 in rat brain membranes. These binding sites for putative Ca2+ channel inhibitors are present in rat heart membranes and have the same characteristics as those in rat brain membranes. These results are discussed in relation with the mechanism of tibalosine antihypertensive effect.

Animals↗
PubMed1984

Antihypertensive activity of tibalosine (CP 804 S) in the rat. Possible involvement of a central alpha 1-adrenergic receptor blockade.

The effect of tibalosine (CP 804 S) on systolic blood pressure and heart rate of unanaesthetized normotensive, spontaneously hypertensive (SHR) and DOCA-salt and Goldblatt hypertensive rats has been examined. After a single oral dose, tibalosine (1.9 to 15 mg/kg) elicited dose-dependent reductions in blood pressure in the four models tested. These reductions are accompanied by a tachycardia except in the SHR where no variation in heart rate is observed. The same result is obtained in SHR after oral, i.v. or i.c.v. administration. After repeated treatment (9 to 14 weeks), the blood pressure lowering effect of tibalosine (10 mg/kg, p.o.) is observed only in hypertensive rats. No variation in heart rate is observed in normotensive, DOCA-salt and Goldblatt rats. A significant bradycardia is observed in the SHR. The antihypertensive effect of tibalosine in SHR is suppressed by naloxone, like that of clonidine and unlike that of prazosin. The present study suggests that the antihypertensive activity of tibalosine is at least partly centrally mediated.

Administration, Oral↗
PubMed1984

[Byler's disease. Ultrastructural study. Apropos of a case in an infant].

A case of familial cholestasis with cirrhosis is described in a 8 months old boy, presenting with hepatosplenomegaly, portal hypertension, dramatic pruritus, and fluctuating icterus of early post-natal onset. Biological data include positive hepatocyte retention test, with mild hepatocyte cytolysis, without patent hepatocyte insufficiency. The discrepancy between the clinical symptoms and a slight elevation of bilirubin partially conjugated, the absence of elevated blood cholesterol, the absence of evidence of antigen or antibody of virus A or B, the marked elevation of blood biliary acid lead to the suspicion of Byler disease. A liver biopsy with ultrastructural study shows a thickening of the ectoplasm, and the presence of microfilament material in the lumen of partially broken villi. Comparisons are made with the 4 other cases of Byler disease with E.M. study documented in the literature.

Bile Acids and Salts↗
PubMed1983

The adenylate cyclase activity in heart membranes from normotensive and spontaneously hypertensive rats, after chemical sympathectomy, suggests the presence of presynaptic secretin receptors.

Normotensive (WKY) and spontaneously hypertensive (SHR) male adult rats were sacrificed 2 and 3 weeks after 6-hydroxydopamine treatment. Untreated WKY and SHR rats served as controls. In rat heart membranes from WKY rats, 6-hydroxydopamine treatment increased guanosine 5'-O-(2-3-imido)-triphosphate (Gpp(NH)p)-, NaF-, D,L-isoproterenol- and glucagon-stimulated adenylate cyclase activities by 18-38% while secretin stimulation was unaffected. In heart membranes from SHR rats, Gpp(NH)p, NaF, D,L-isoproterenol, or glucagon stimulation of the enzyme was similarly increased by 14-38% whilst the low secretin responsiveness which is characteristic of these animals decreased even further (by 24-47%). These results are consistent with: (1) an up regulation of postsynaptic beta-adrenergic receptors coupled to adenylate cyclase after degeneration of adrenergic nerves, and (2) a differential response of secretin receptors coupled to adenylate cyclase in the two strains of rats: there was no change in WKY rats and a decreased response in SHR rats. The possible presence and contribution of presynaptic secretin cardiac receptors is considered.

Adenylyl Cyclases↗
PubMed1983

Conversion of orally administered 2-n.pentylaminoacetamide into glycinamide and glycine in the rat brain.

Male Sprague Dawley albino rats were treated orally with 2-n.pentylaminoacetamide (10 to 100 mg/kg b.wt). This oral administration provoked a dose-related and time-dependent accumulation of glycinamide in forebrain, cerebellum, and medulla, and to increased levels of glycine in the three brain areas, and of serine in medulla. In kidney, liver and plasma, the accumulation of glycinamide was lower and there was no increase in glycine and serine levels. With a dose of 100 mg/kg b.wt, 28% of the drug were eliminated unchanged and 16% as glycinamide, in urines collected for 24 h. In all tissues examined, 2-n.pentylaminoacetamide and glycinamide levels peaked at 1 h and were nil again after 24 h, the ratio of 2-n.pentylaminoacetamide over glycinamide decreasing more rapidly in brain than in kidney and liver. Contrasting with the effects of 2-n.pentylaminoacetamide, the oral administration of glycinamide (66 mg/b.wt) led, 2 hours later, to similar low rises of glycinamide in plasma and brain. In another control experiment, the intraperitoneal injection of a large dose of glycine (450 mg/kg b.wt) provoked, 30 min later, modest rises of glycine levels in the central nervous system that merely reflected a contamination by plasma glycine.

Administration, Oral↗
PubMed1983

Increased number of high-affinity muscarinic receptors in rat heart after phenylhydrazine treatment.

The effect of phenylhydrazine-induced heart hypertrophy on muscarinic cholinergic binding sites was studied in heart membranes by determining total (with [3H]NMS) and high-affinity (with [3H]Oxo-M) binding sites and estimating low-affinity binding sites by difference. Phenylhydrazine induced an increased concentration of high-affinity binding sites without affecting the concentration of low-affinity binding sites. The KD values for the ligands were unaffected.

Animals↗
PubMed1983

Effects of full and partial beta-adrenergic agonists and antagonists on human lung adenylate cyclase.

The beta-adrenergic stimulation of adenylate cyclase in membranes from human lung was compared to that of adenylate cyclase in membranes with a majority of beta 2-adrenergic receptors (from rat lung) and in membranes with a homogeneous population of beta 2-adrenergic receptors (from rat erythrocytes and reticulocytes). In terms of adenylate cyclase stimulation, three full agonists (isoproterenol, epinephrine and norepinephrine), four partial agonists (procaterol, salbutamol, fenoterol and zinterol), and four antagonists (propranolol, metoprolol, atenolol and practolol) were tested. The potency (Kact or Ki) of the eleven beta-adrenergic agents, and the Hill coefficient (of 1) for the four antagonists tested indicated that the activation of human lung adenylate cyclase occurred through receptors of the beta 2-subtype only. Partial beta-adrenergic agonists were efficiently discriminated by the human lung preparation, as shown by distinct intrinsic activities. The mediocre efficacy and the relatively low potency of all beta-adrenergic agonists on adenylate cyclase suggested a relatively low density of beta 2-adrenergic receptors, as compared to the enzyme density.

Adenylyl Cyclase Inhibitors↗
PubMed1983

Inhibition of forskolin-stimulated cardiac adenylate cyclase activity by short-chain alcohols.

The diterpene forskolin stimulated rat cardiac adenylate cyclase activity at least 20-fold and potentiated the effect of NaF. The stimulatory effect of forskolin was reduced in the presence of Gpp(NH)p. Ethanol markedly reduced the stimulation of adenylate cyclase by forskolin while potentiating NaF and Gpp(NH)p stimulation. The inhibitory effect of ethanol on forskolin stimulation appeared to be of a mixed type with both a competitive and a non-competitive component. Three other short-chain linear alcohols (methanol, propanol, butanol) also inhibited forskolin-stimulation, this effect being proportional to the number of carbon atoms.

Adenylyl Cyclases↗
PubMed1983

Topographical distribution of the secretin- and VIP-stimulated adenylate cyclase system in the heart of five animal species.

Adenylate cyclase stimulation by secretin and VIP was compared to the effect of glucagon, D,L-isoproterenol, Gpp[[NH]p, and NaF in atria and ventricles from rat, guinea pig, rabbit, dog and Cynomolgus monkey. In rat ventricular membranes, secretin was a better stimulant than VIP and was as active as D,L-isoproterenol. In rat auricular membranes both peptides were inactive. In guinea pig and rabbit heart membranes (ventricular and auricular) VIP and secretin were inactive. In dog and monkey atria, VIP stimulation of adenylate cyclase was comparable to that of D,L-isoproterenol, secretin being inactive. In dog ventricles, VIP was less efficient than D,L-isoproterenol, secretin being inactive. In monkey ventricles, by contrast, VIP was slightly more efficient than D,L-isoproterenol, secretin having a small effect only in left ventricles. The present results established a clear difference between animal species with respect to the efficacy of the peptides of the secretin/VIP family: the presence of "secretin-preferring" receptors in rat heart contrasted with the presence of "VIP-preferring" receptors in dog and monkey heart. Our results in dog and monkey hearts suggest that VIP might be a candidate for a physiological control of heart function.

Adenylyl Cyclases↗
PubMed1983

Thermodependence of basal and stimulated cardiac adenylate cyclase activity in normotensive and spontaneously hypertensive rats.

The cardiac adenylate cyclase activity from normotensive and spontaneously hypertensive (SHR) rats was studied as a function of temperature between 17 degrees and 37 degrees C. Arrhenius plots of adenylate cyclase activity displayed a break around 31 degrees C when tested under basal conditions or in the presence of GTP but were linearized after activation with p[NH]ppG, NaF, secretin, glucagon or isoproterenol. The energy of activation of adenylate cyclase activity in the presence of GTP (9.5 +/- 0.5 kcal/mol) was significantly lower than in the presence of p[NH]ppG (17.7 +/- 0.8 kcal/mol). A hormone was without effect on the energy of activation observed with either GTP or p[NH]ppG but the simultaneous presence of hormone and nucleotide increased markedly the activity of the enzyme. The energies of activation were analyzed in terms of variation of enthalpy and entropy and discussed in relation with the process of activation and coupling of the guanine nucleotide regulatory protein. These thermodynamic characteristics were similar in cardiac membranes from normotensive and spontaneously hypertensive rats, suggesting that the impairment of hormone-stimulated adenylate cyclase activity observed in the heart membranes of hypertensive rats was not a consequence of a defect in the activation process of the enzyme.

Adenylyl Cyclases↗
PubMed1983

[Computerization of a bank of platelets with HLA phenotype and preserved at -196 degrees C].

In order to complete the logistics of the unit cytapheresis, we have developed a decision helping system which rests upon the computer management of -196 degrees C cryopreserved HLA type platelets. The hardware used is a micro-computer equipped with two floppy disks and a printer. Two files have been created: namely "Product" and "Patient". Data relating to 800 platelet concentrates may be recorded on a floppy disk. The software which has been developed has several functions: 1 - The input of the parameters of a HLA type concentrate with the possibility of reservation for the given recipient; 2 - The print out of the bank's stock; 3 - The selection and the reservation of HLA matched platelets according to the recipient; 4 - The print out of concentrates allocated to each patient, it is possible to thaw out chosen platelet concentrate and a thawing report is printed out, thus enabling one to locate the concentrate in the bank. Thanks to this "aid in decision making", the management of - 196 degrees C cryopreserved HLA type platelets may be carried out. The proposed software allows an one line answer for any emergency transfusion case. Considering the recipient HLA typing the suitable best match platelet concentrates are instantly transfused or save.

Blood Transfusion↗
PubMed1983

Selective alteration of secretin-stimulated cardiac adenylate cyclase activity in streptozotocin-diabetic rats.

Secretin stimulation of adenylate cyclase activity in heart membranes was selectively altered in streptozotocin-diabetic adult male rats suffering from moderately severe diabetes, 40 days after i.v. streptozotocin administration (40 mg/kg body weight). The efficacy of secretin was reduced by 55% whilst its potency was unaffected. By contrast, the stimulation of adenylate cyclase by NaF, GTP, Gpp(NH)p, D,L-isoproterenol, and glucagon remained normal. The present data, together with the markedly reduced secretin response of cardiac adenylate cyclase in genetically obese (fa/fa) Zucker rats might indicate that hypoinsulinemia and insulin resistance both reduce the number of secretin receptors coupled to the adenylate cyclase system, an alteration whose contribution to diabetic cardiomyopathy remains to be determined.

Adenylyl Cyclases↗
PubMed1983

Effect of purified somatomedins on thymidine incorporation into lectin-activated human lymphocytes.

These data describe the effects of purified preparations of several growth factors on thymidine incorporation into phyto-haemagglutinin-activated (PHA) human lymphocytes. The somatomedins selected for this study included human somatomedins A and C, insulin-like growth factors (IFG1 and IGF2) and multiplication stimulating activity (MSA). Assays were carried out with and without serum. Complementary assays were performed with a low-molecular serum ultrafiltrate added to somatomedin C and to MSA. We found that all the peptides tested, except MSA, stimulated thymidine incorporation into PHA-activated lymphocytes in a dose-dependent manner, even though different doses were required to obtain a response. The data reported point out the multiplicity and the interrelationships of the serum factors involved in the stimulation of human cells growth.

Animals↗
PubMed1983

The human heart beta-adrenergic receptors. I. Heterogeneity of the binding sites: presence of 50% beta 1- and 50% beta 2-adrenergic receptors.

Beta-adrenergic receptors were characterized in a particulate fraction of human auricles obtained from patients operated upon for coronary insufficiency or valvular disease. [125I] Hydroxybenzylpindolol binding was evaluated in terms of kinetics; KD and Bmax values; and inhibition of binding in the presence of 10 microM GTP and of increasing concentrations of four nonselective agonists giving a Hill coefficient of 1 (isoproterenol, salbutamol, fenoterol, and epinephrine), of two nonselective antagonists giving a Hill coefficient of 1 (pindolol and propranolol), and of a series of selective drugs giving a Hill coefficient of 0.60-0.72 that included three beta 1-selective antagonists (practolol, metoprolol, and atenolol) and two beta 2- selective agonists (procaterol and zinterol). KD values for all drugs were compatible with the coexistence in membranes from human auricles of beta 1- and beta 2-adrenergic receptors, the relative proportions of receptors of each subclass being approximately the same.

Adrenergic beta-Agonists↗
PubMed1983

The human heart beta-adrenergic receptors. II. Coupling of beta 2-adrenergic receptors with the adenylate cyclase system.

The beta-adrenergic stimulation of adenylate cyclase in membranes from human auricles, ventricles, and fetal heart was compared with the binding properties of beta-adrenergic receptors in human auricles. In terms of adenylate cyclase activation, three full agonists (isoproterenol, epinephrine, and norepinephrine), four partial agonists (procaterol, salbutamol, fenoterol, and zinterol), and four antagonists (propranolol, metoprolol, atenolol, and practolol) were tested. The beta-adrenergic activation of adenylate cyclase in membranes from rat heart (with a majority of beta 1-adrenergic receptors), rat erythrocytes, and rat reticulocytes (with a homogeneous population of beta 2-adrenergic receptors) served as reference. The reactivity of human heart adenylate cyclase, estimated by the Kact or Ki values of 11 beta-adrenergic agents, indicated that the activation of this enzyme occurred through receptors of the beta 2-subtype only. Receptors of the beta 1-subtype (50% of the total population) were not coupled to the enzyme.

Adenylyl Cyclases↗