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Biomedical subjects

P Lechat

Publications and source records attributed to P Lechat.

At least 343 records · Page 19Linked to original sources
PubMedDate not supplied

[Effectiveness and tolerance of digitaloid treatment in cardiac insufficiency].

Ever since digitaloids have been used in the treatment of cardiac failure, their effectiveness in cases with sinus rhythm has been controversial. Nevertheless, their inotropic effect at therapeutic concentrations has been well demonstrated in man. The haemodynamic benefit in cardiac failure is greater the more severe the condition. Recent studies have shown that the patients who respond best to digitaloid treatment are those with chronic severe heart failure with ventricular dilatation, reduction in the ejection fraction and a gallop on auscultation. In contrast, when digitaloid treatment is suspended in patients with functional class II or III ischaemic heart failure, there does not appear to be any aggravation provided diuretic and/or vasodilator treatment is continued.

Adenosine Triphosphatases↗
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

[Aggregation of macrophages by a human lymphokine (MAgF). Role of the eicosanoid system].

Peritoneal exudate cells aggregate when exposed to the lymphokine Macrophage Aggregating Factor (MAgF). The role of prostaglandins in the aggregation of these cells has been investigated with a quantitative assay. Results are discussed in the context of the mode of action of the migration inhibiting factor (MIF) and of the other non immune aggregating stimuli such as C5a and fMLP. Prostaglandins E1, E2, and F2 alpha alone did not cause aggregation of macrophages but partially inhibited the MAgF aggregation of macrophages and this effect was not different from the one obtained with MAgF. MAgF, calcium ionophore A23187 and arachidonic acid induced aggregation were blocked by 5, 8, 11, 14-eicosatetraynoic acid, an inhibitor of arachidonic acid metabolism, by indomethacin (10(-4), 10(-6) M) by corticosteroids (dexamethazone, methylprednisolone, hydrocortisone) but not by aspirin (10(-2), 10(-4) M) nor by phenylbutazone (10(-4), 10(-5) M). These results suggest a causal relationship between MAgF induced macrophage aggregation and that due to other stimuli with respect to the derivatives of arachidonic acid. The lipoxygenase pathways metabolites stimulate aggregation whereas the cyclo-oxygenase pathways metabolites inhibit it.

Anti-Inflammatory Agents↗
PubMedDate not supplied

[Electrocardiographic effects and antiarrhythmic action of 1200 mg of oral amiodarone per day].

The authors administered 1 200 mg of amiodarone orally to 30 patients with paroxysmal supraventricular and ventricular arrhythmias for a period of 6 days. They evaluated the electrocardiographic modifications induced on the surface ECG as well as the anti-arrhythmic action which was assessed by continuous Holter ECG monitoring and endocavitary electrophysiological investigations. They found that the sinus rhythm was slowed by 22%, that the PR interval was prolonged by 22%, that the QTc interval was increased by 13.5% and that there were alterations in ventricular repolarisation in 48% of cases. These ECG modifications were maximal between the 5th and 7th days. The amiodarone controlled the arrhythmia in 57% of cases. Independent of the nature of the arrhythmia, the anti-arrhythmic effect appeared after a mean of 3.9 +/- 1.8 days. There was no significant relationship between the electrocardiographic modifications and the anti-arrhythmic effect. In three cases (10%), major side effects were observed, related to depression of sinus automatism. They only appeared after the 6th day. Thus, a loading dose of 1 200 mg/day of amiodarone p.o. can be administered without fear of major side effects for 4 to 5 days. Such treatment will control about 60% of cases of severe paroxysmal arrhythmias after 4 days.

Administration, Oral↗
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↗
PubMedDate not supplied

[Myocardial ischemia detected by Holter monitoring: analysis of therapeutical trials realised in stable angina].

Silent myocardial ischaemia is the most frequent consequence of coronary artery disease and occurs in almost 70 per cent to 80 per cent of ischaemic episodes. In some studies, it has some predictive value of cardiovascular events either in stable or unstable angina or after myocardial infarction. In this last case, one year mortality is 30 per cent and 11 per cent respectively with and without silent ischaemia that has been recorded on the 8th day after myocardial infarction. This review has focused on controlled studies in patients with angina and Holter recorded ischaemia. Nitrates are very likely to be active substances on Holter recorded angina but no controlled studies have been performed to really demonstrate it. The efficacy of beta-blocking agents is well established with a 60 per cent reduction in the number of ischaemic events and a 80 per cent reduction in total ischaemic duration. Nifedipine efficacy appears lower than that of beta-blockers with an evaluated mean reduction of 39 per cent for the number of events and of 43 per cent for duration of episodes. Diltiazem induces a 48 per cent reduction of both ischaemic parameters. For drug associations, addition of a calcium antagonist to a beta-blocking agent provides only little benefit. The relationship between anti-ischaemic efficacy and long term prevention of cardiovascular events remains to be established for a given anti-ischaemic therapy.

Adrenergic beta-Antagonists↗