Search PubMed⌕ Search

Biomedical subjects

M C Auclair

Publications and source records attributed to M C Auclair.

54 records · Page 3Linked to original sources
PubMedDate not supplied

Relative negative inotropic potencies of nine calcium channel blockers in cultured heart cells.

The direct inhibitory effects on contractility and beating rate of the calcium channel blockers diltiazem, verapamil and dihydropyridine derivatives nicardipine, nifedipine, nitrendipine, PY 108-068, (+/- ) PN 200-110 and its 2 stereoisomers, were compared in cultured chick embryo ventricular cells. In spontaneously beating cells, the negative inotropic and chronotropic potencies of nicardipine, nifedipine, nitrendipine and PY 108-068 were not significantly different. The inhibitory effects of verapamil, nifedipine and nicardipine were studied in cells electrically driven at a frequency close to their spontaneous beating rate: verapamil, nifedipine and nicardipine had similar negative chronotropic potencies; when the rate of stimulation was increased 1.5 and 2-fold, a frequency-dependent inhibitory effect on contraction was shown for verapamil, but not for nifedipine and nicardipine. Therefore, in our model, where the effects of beating rate on the amplitude of contraction were taken into account, no significant difference in the direct negative inotropic potenties of nifedipine and nicardipine was shown.

Animals↗
PubMedDate not supplied

[Cardiac disorders induced by mianserin in guinea pigs. Comparison with imipramine].

Infusion of mianserin to anesthetized guinea-pigs induced electrocardiographic changes (auriculo-ventricular and intraventricular conduction lenghthening, bradycardia, QRS axis and T axis rotations) quite identical to those induced by imipramine. However they appeared later and mianserin produced cardiac arrest at higher dose (133 mg/kg) than did imipramine (73 mg/kg). In vitro, increasing concentrations of mianserin suppressed the electrical response of stimulated, isolated ventricular heart strips, but this suppression was obtained by a higher concentration (172 micrograms/ml) than with imipramine (80 micrograms/ml). Transmembrane potentials were not affected by a 5 or 10 micrograms/ml mianserin or a 5 micrograms/ml imipramine perfusion. With 20 micrograms/ml mianserin or 10 micrograms/ml imipramine, only a reduced duration of the action potential was obtained. With 50 micrograms/ml mianserin or 20 micrograms/ml imipramine, the resting potential was reduced. However, with imipramine only it was preceded by a decrease in the maximal velocity of depolarisation. These results show that mianserin induces transmembrane permeability changes which appear to differ from and to be less marked than those induced by imipramine. Molar sodium bicarbonate reversed in vivo and in vitro the electrophysiologic changes elicited either by mianserin or by imipramine, but with mianserin the transient improvement was followed by an aggravation of the cardiac troubles.

Animals↗
PubMedDate not supplied

[Decrease of the hypertensive responses to phenylephrine in the rat submitted to a sublethal dose of E. coli endotoxin. Restoration by indomethacin (author's transl)].

E. Coli endotoxin was injected by i.v. route to rats at a dose immediately lower than the minimal lethal dose. Assays were performed on anesthetized rats (urethane 1 g/kg i.p.). The carotid arterial pressure was recorded 1, 2, 4, 16 and 24 hours after endotoxin administration, and hypertensive responses to three successive doses of phenylephrine (2; 5 or 10 micrograms/kg i.v.) was measured until return to initial values. Compared to control rats the hypertensive responses in the endotoxin-treated rats were depressed. This depression was evident at the first hour following endotoxin administration and was maintained at least for four hours. This lower response was improved by a treatment of the rats with indomethacin (10 mg/kg i.v.) when this drug was administered half an hour before, or concomitantly with endotoxin. When indomethacin (10 mg/kg) was given two hours after endotoxin the improvement was less marked. So did indomethacin at 5 mg/kg dose level. Indomethacin alone did not potentiate the pressive responses to phenylephrine. These results show that the endotoxin-induced decrease in the hypertensive responses to phenylephrine does not appear to depend on its hypotensive or lethal effects. It can be brought together with the low cardiovascular responses to different drugs found in animals under endotoxin shock. These results show moreover that an early increase in prostaglandin synthesis under the influence of endotoxin may be involved in this depressant effect.

Animals↗