Biomedical subjects

L Vernhet

Publications and source records attributed to L Vernhet.

22 records · Page 2Linked to original sources

PubMed1995

Incorporation of arachidonic and eicosapentaenoic acids into phospholipids of non-transformed and spontaneously-transformed rat liver epithelial cells: effects on DNA-synthesis.

We compared the incorporation of arachidonic acid (AA) and eicosapentaneoic acid (EPA) into phospholipids of non-transformed (NT-) and spontaneously-transformed (T-) rat liver epithelial cells (RLEC), and their consequences on DNA-synthesis. In NT-cells, both radioactive fatty acids were preferentially incorporated into phosphatidylcholine (PC). In T-cells, in contrast, AA was predominantly incorporated into phosphatidylethanolamine (PE), whereas EPA remained preferentially incorporated into PC. After pulse labelling, we observed in both cell types a progressive decrease in AA- and EPA-labelled PC associated with an increase in AA- and EPA-labelled PE. Preincubation of NT-cells with increasing concentrations of AA or EPA (0.1 microM to 20 microM) resulted in a concentration-dependent DNA-synthesis stimulation with a stronger effect of AA compared with EPA. In T-cells, the same treatment had no effect on DNA-synthesis.

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PubMed1993

Reproducibility of the model of induced ventricular tachycardia in conscious dogs with infarction.

The canine model of ventricular tachycardias (VT) induced by programmed stimulation is used routinely in several laboratories to test antiarrhythmic drugs. The aim of the present study was to determine the rate of success and reproducibility of this model. We analyzed a group of 58 dogs that underwent a 2-hr occlusion and were submitted to programmed electrical stimulation at least 4 days after the surgery. Only 29 dogs (50%) were inducible and included in the study, as 22 dogs died following myocardial infarction, and seven dogs were never inducible. Out of 130 trials, 92 (70%) performed on inducible dogs were positive with 11% of nonsustained ventricular tachycardias, 63% of sustained monomorphic ventricular tachycardias, and 26% of ventricular fibrillation. Inducibility decreased over time in a subgroup of 19 dogs that was submitted to four trials during the first month after the infarction (68% of inducible dogs versus 46% in trials 1 and 4, respectively). Ventricular effective refractory period decreased significantly from 146 +/- 7 msec at trial 1 to 114 +/- 6 msec at trial 4, and the severity of the induced ventricular tachycardias increased. This variability should be considered when planning studies on antiarrhythmic drugs in this model.

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PubMed1993

Antiarrhythmic effect of a sotalol-mexiletine combination on induced ventricular tachycardia in dogs.

Mexiletine was recently shown to antagonize the effects of sotalol on repolarization of canine Purkinje fibers. The significance of this interaction for the antiarrhythmic properties of these drugs remains unknown. The antiarrhythmic effects of sotalol and mexiletine alone and in combination on induced ventricular tachycardias (VTs) were assessed in 20 conscious dogs with chronic infarction. Electrophysiological measurements and programmed stimulation were performed before and after the infusion of sotalol (4 mg/kg) or mexiletine (4 mg/kg), and after infusion of the combination. The electrophysiological parameters didn't change after mexiletine. Sotalol alone and the combination both similarly prolonged the QT interval and VERP. Induction of VT by programmed stimulation was not prevented by mexiletine, but the cycle length of monomorphic VT was increased in 7 of 10 dogs. The induction of VT was prevented by sotalol (11/16 dogs), but VTs were not slowed significantly. Sotalol plus mexiletine prevented VT as did sotalol alone (11/16 dogs). The combination also increased the cycle length of VT in all eight dogs with monomorphic VT. Thus, the antagonism shown in vitro appears to have no consequences in this model. On the contrary, the sotalol-mexiletine combination showed some additive antiarrhythmic effects on induced VT in dogs.

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PubMedDate not supplied

Furosemide-sensitive K+ transport in transformed and nontransformed rat liver epithelial cells: regulation by protein kinase C and involvement in cell growth.

Using Rb+ as a K+ tracer and atomic absorption spectrophotometry for measuring the Rb+ stable isotope, we studied K+ transport systems and their regulation by protein kinase C in nontransformed and spontaneously transformed rat liver epithelial cells. Ouabain-sensitive Na+/K(+)-ATPase and the furosemide-sensitive Na+/K+/Cl- cotransport had comparable activity ratios in both cell types (0.92 and 1 in nontransformed and transformed rat liver epithelial cells, respectively). The protein kinase C activators, dioctanoylglycerol and phorbol myristate acetate, partly inhibited the Na+/K+/Cl- cotransport in both cell types but their effect was stronger in nontransformed cells, suggesting that, in transformed cells, the Na+/K+/Cl- cotransport had partly lost the ability to be inhibited by protein kinase C. In both cell types, phorbol myristate acetate had little and dioctanoylglycerol had no inhibitory effect on Na+/K(+)-ATPase. Furosemide (1 mM) partly inhibited the [3H]thymidine incorporation in both cell types, suggesting an involvement of the Na+/K+/Cl- cotransport in rat liver epithelial cell growth.

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