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C Massé

Publications and source records attributed to C Massé.

At least 19 recordsLinked to original sources
PubMed2001

Modulation of alpha-ENaC and alpha1-Na+-K+-ATPase by cAMP and dexamethasone in alveolar epithelial cells.

cAMP and dexamethasone are known to modulate Na+ transport in epithelial cells. We investigated whether dibutyryl cAMP (DBcAMP) and dexamethasone modulate the mRNA expression of two key elements of the Na+ transport system in isolated rat alveolar epithelial cells: alpha-, beta-, and gamma-subunits of the epithelial Na+ channel (ENaC) and the alpha1- and beta1-subunits of Na+-K+-ATPase. The cells were treated for up to 48 h with DBcAMP or dexamethasone to assess their long-term impact on the steady-state level of ENaC and Na+-K+-ATPase mRNA. DBcAMP induced a twofold transient increase of alpha-ENaC and alpha1-Na+-K+-ATPase mRNA that peaked after 8 h of treatment. It also upregulated beta- and gamma-ENaC mRNA but not beta1-Na+-K+-ATPase mRNA. Dexamethasone augmented alpha-ENaC mRNA expression 4.4-fold in cells treated for 24 h and also upregulated beta- and gamma-ENaC mRNA. There was a 1.6-fold increase at 8 h of beta1-Na+-K+-ATPase mRNA but no significant modulation of alpha1-Na+-K+-ATPase mRNA expression. Because DBcAMP and dexamethasone did not increase the stability of alpha-ENaC mRNA, we cloned 3.2 kb of the 5' sequences flanking the mouse alpha-ENaC gene to study the impact of DBcAMP and dexamethasone on alpha-ENaC promoter activity. The promoter was able to drive basal expression of the chloramphenicol acetyltransferase (CAT) reporter gene in A549 cells. Dexamethasone increased the activity of the promoter by a factor of 5.9. To complete the study, the physiological effects of DBcAMP and dexamethasone were investigated by measuring transepithelial current in treated and control cells. DBcAMP and dexamethasone modulated transepithelial current with a time course reminiscent of the profile observed for alpha-ENaC mRNA expression. DBcAMP had a greater impact on transepithelial current (2.5-fold increase at 8 h) than dexamethasone (1.8-fold increase at 24 h). These results suggest that modulation of alpha-ENaC and Na+-K+-ATPase gene expression is one of the mechanisms that regulates Na+ transport in alveolar epithelial cells.

Animals↗
PubMed1993

[Non-surgical treatment of Dupuytren disease using needle fasciotomy].

Short-term and five-year outcomes after nonsurgical treatment of Dupuytren's contracture by needle fasciotomy were studied. Among the 138 patients who were evaluated, 90 (123 hands) were seen five years after the procedure. Outcome was excellent or good in 81% of cases in the short term and 69% of cases after 5 years. Adverse events included skin breaks (20 hands, 16% of cases), digital dysesthesia due to nerve damage (3 patients, 2% of cases), and local infection (3 patients, 2% of cases). Five-year recurrence rate was 50.4%. These findings demonstrate the value of needle fasciotomy especially in the early stages of Dupuytren's disease.

Dupuytren Contracture↗
PubMed1990

Bupivacaine-induced slow-inward current inhibition: a voltage clamp study on frog atrial fibres.

The effects of various concentrations of bupivacaine on the characteristics of the slow-inward current (isi) were studied over a ten-minute period on isolated frog atria. At a concentration of 10(-7) M, bupivacaine did not modify isi. At 10(-6) M, the maximal amplitude of the slow-inward current (i max) was depressed by 11 per cent. At 10(-5) M, i max was depressed by 24.5 per cent, the time-to-peak current value (tpeak) was increased by 13.4 per cent and the inactivation time constant (tau in) by 29.8 per cent. At 10(-4) M, i max was depressed by 32.9 per cent, tpeak increased by 30.4 per cent and tau in by 58.7 per cent. In conclusion, bupivacaine produced only moderate inhibition of the slow-inward current. The findings might explain the decline in sinus impulse formation with sinus bradycardia, and the slowing of atrio-ventricular node conduction produced by bupivacaine. However, the decrease in contractility previously reported does not seem to be due only to inhibition of the slow-inward current.

Action Potentials↗
PubMed1989

In vitro study on mechanisms of bupivacaine-induced depression of myocardial contractility.

Although several mechanisms have been proposed to explain bupivacaine cardiotoxicity, the predominant effect remains to be determined. In this study, we used an isolated rabbit right atrial model that reproduces the effects on inotropic and chronotropic functions induced by 0.5 micrograms/mL bupivacaine; then we tried to counteract these events by electrical stimulation or by addition of CaCl2 or adenosine triphosphate (ATP) to the bathing solution. Contractile force was dramatically depressed by bupivacaine alone (-68%), even when the preparation was paced (-59%). CaCl2 partially counteracted this decrease (-37%). Inotropic function was almost completely restored (-9%) when ATP was added before administration of bupivacaine. Inhibition of energy metabolism seems to be a major explanation for bupivacaine cardiotoxicity.

Adenosine Triphosphate↗
PubMed1987

Evidence for a class 4 effect of cibenzoline "in vivo".

In anesthetized dogs, it has already been shown that cibenzoline (4 mg/kg i.v.) possesses class 1 anti-arrhythmic properties. In this work, the cardiac electrophysiologic effects of cibenzoline (1 mg/kg i.v.) were studied before and after propranolol (0.2 mg/kg i.v.) treatment. Cibenzoline caused a slight tachycardia, a reduction of conduction velocity in the His-Purkinje system and in the ventricle, but no significant effects in the atria and the atrioventricular node were detected. On the contrary, when dogs were given the beta-adrenoceptor blocking agent propranolol, cibenzoline produced major effects in the slow response structures, especially in the sinus node and the atrioventricular node (bradycardia and depression of the atrioventricular nodal conduction). No further effects were observed on the His-Purkinje system and ventricle as compared to administration of cibenzoline alone. In dogs, cibenzoline given i.v., had no effects on the slow response systems, probably because of sympathetic nervous system intervention since the class 4 effects of cibenzoline appeared after beta-adrenoceptor blockade.

Anesthesia↗
PubMed1984

Cardiac electrophysiological effects of cibenzoline by acute and chronic administration in the anesthetized dog.

The electrophysiological effects of cibenzoline on the myocardium of the anesthetized dog were studied by the endocavitary catheter method. Plasma cibenzoline levels were measured throughout. The cibenzoline effects on the sinus rate were negligible. The corrected sinus recovery time was significantly prolonged only following chronic oral administration. Atrial refractory periods were significantly increased only at the fifth minute following acute intravenous administration and after chronic oral treatment. The intranodal conduction time (AH) and the refractory periods in atrio-ventricular node were slightly modified or not at all. On the other hand, intraventricular and His-Purkinje (HV) conduction times, ventricular refractory periods and QRS duration were strongly increased following acute or chronic administration. This would imply a principal effect on the rapid kinetics sodium entry current. Nevertheless, the very marked effect upon this current could, under the experimental conditions adopted, have masked a lesser action upon other membrane permeabilities, involved in other myocardial structures.

Administration, Oral↗
PubMed1975

Effects of antiarrhythmic drugs on cardiac membrane conductances; a study using the Hodgkin and Huxley mathematical model.

A study in voltage clamp conditions of the modifications of the cardiac membrane conductances by quinidine sulfate has been carried out on frog atrial fibers by means of the double sucrose gap technique. The computation of the parameters related to the conductances has been done according to the Hodgkin and Huxley mathematical model proposed in 1952. The computed conductances concern the sodium conductance, the calcium conductance, and the total delayed conductance. A decrease of all of the studied conductances is observed in the presence of quinidine sulfate. This drug also mainly induced a slowing down of several activation, inactivation, and reactivation kinetics. The results obtained allow a more detailed explanation of the mechanism of action of quinidine sulfate in the membrane. Although quinidine is known to possess antiarrhythmic properties, the exact mechanisms of its action are not clear. The present study was therefore undertaken to provide some information on this point.

Animals↗