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Biomedical subjects

M Finet

Publications and source records attributed to M Finet.

29 records · Page 2Linked to original sources
PubMed1989

The protective action of R56865 against ouabain-induced intoxication in rat heart isolated atria and ventricles.

The action of R56865 has been examined on the contractile effects produced by ouabain concentrations interacting with high (3 microM) and low (300 microM) affinity digitalis receptors on electrically stimulated ventricular strips isolated from rat. R56865 1 microM reduced the increase in resting tension produced by ouabain 300 microM and left unalterated the inotropic effect evoked by ouabain 3 and 300 microM that was reduced by higher concentrations (3 and 6 microM) of R56865. The action of R56865 was also studied on ouabain-induced intoxication in electrically stimulated and spontaneously beating atria of rat. On electrically stimulated (3 Hz) whole atria, R56865 0.3 microM reduced the maximal increase in resting tension produced by ouabain 300 microM and delayed the time to onset of the ouabain-induced arrhythmias but did not affect ouabain's inotropic effect. Higher concentrations of R56865 were required to reduce the inotropic effect of ouabain. The protective action of R56865 against ouabain-induced intoxication was most pronounced on spontaneously beating atria where it reduced spontaneous rate of beats. Experiments in electrically driven left atria indicated that only a part of the protective effect of R56865 could be related to its bradycardic action. The effect of R56865 was also examined on ouabain-induced inhibition of sodium pump in human red blood cells. R56865 6 microM did not modify the inhibition produced by ouabain (from 0.3 to 10 nM), this indicates that the protective action of R56865 against ouabain-induced intoxication is not due to an interaction with the inhibitory effect of ouabain on sodium pump.

Animals↗
PubMed1989

Pharmacology of endothelin-1 in isolated vessels: effect of nicardipine, methylene blue, hemoglobin, and gossypol.

Sensitive bioassay tissues for porcine endothelin-1 (ET-1) were developed in a cascade superfusion system and in organ baths. Venous preparations of the rabbit and rat were more sensitive than arterial preparations. ET-1 had a different pharmacological profile than Bay K 8644 on the various preparations. Nicardipine (0.1-1 microM) abolished the responses to Bay K 8644 without affecting those induced by ET-1. Thus, ET-1 contracts venous and some arterial vessels via specific receptors or channels that differ from dihydropyridine-sensitive calcium channels. Methylene blue and hemoglobin potentiated responses to ET-1 in endothelium-denuded venous vessels, whereas gossypol had no effect.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1987

The actions of nifedipine and nisoldipine on the contractile activity of human coronary arteries and human cardiac tissue in vitro.

We have studied the action of nifedipine and nisoldipine on the contractile activity of human isolated coronary arteries and human isolated auricular and ventricular muscles. Nisoldipine depressed dose dependently the spontaneous rhythmic contractions displayed by the coronary artery preparations and at 1 nM abolished these contractions. Nisoldipine was twenty times more potent than nifedipine as an inhibitor of increase in tone induced by depolarization (100 mM K+). The rhythmic activity induced by serotonin (10 microM) was about five times more sensitive to nisoldipine than to nifedipine. In both auricular and ventricular preparations, isoprenaline evoked an increase in the rate of force development and in the rate of relaxation. Nifedipine was five times (ventricular muscles) and ten times (auricular muscles) more potent than nisoldipine as a negative inotropic agent. The present observations in human isolated preparations indicate that nisoldipine shows a higher vascular selectivity than nifedipine.

Adolescent↗
PubMed1986

Selective inhibition by ethylisopropylamiloride of the positive inotropic effect evoked by low concentrations of ouabain in rat isolated ventricles.

The biphasic positive inotropic effect of ouabain has been studied in rat ventricular strips in the presence of ethylisopropylamiloride (EIPA) an inhibitor of Na+/H+ exchange. EIPA (10-20 microM) depressed dose-dependently the high affinity component of the ouabain inotropic effect, whereas it did not significantly modify the low affinity inotropic effect related to high concentrations of ouabain. At the EIPA concentrations studied, there was no observable modification of the inotropic effect of Bay K 8644 (10 nM, 0.3 microM) or of isoprenaline (10 nM, 1 microM). These results indicate that the inotropic effect of ouabain resulting from its interaction with high affinity sites is selectively sensitive to EIPA.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1985

The positive inotropic action of the nifedipine analogue, Bay K 8644, in guinea-pig and rat isolated cardiac preparations.

The inotropic effect of Bay K 8644 has been studied in rat and guinea-pig atria and ventricular strips stimulated at 1 Hz, in a medium containing CaCl2 1.8 mM. The positive inotropic effect at maximal effective concentrations of Bay K 8644 was in the following order: guinea-pig ventricle greater than rat ventricle greater than guinea-pig atria greater than greater than rat atria. In rat preparations, the tension recorded at maximum effective concentrations of Bay K 8644 was similar at three different calcium concentrations (0.7, 1.8, 3.0 mM). The amplitude of the positive inotropic effect evoked by Bay K 8644 increased when atrial and ventricular contractions were reduced by lowering the external calcium concentration. The contractile tension reached in the presence of maximum effective concentrations of Bay K 8644 (3 X 10(-7) -1 X 10(-6) M) was greater than that produced by the maximum effective concentration of external calcium (3 mM) in rat ventricles but not in rat atria. High doses of nifedipine (3 X 10(-7) -1 X 10(-6) M) depressed the contraction of rat atria more than the contraction of rat ventricles. In rat ventricles, nifedipine shifted to the right the inotropic dose-effect curve of Bay K 8644. It is concluded that the interaction between nifedipine and Bay K 8644 occurred at the same binding sites. These sites have some characteristics of the low affinity binding sites of nifedipine and other related dihydropyridines.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1985

Critical role of oxalate restriction in association with calcium restriction to decrease the probability of being a stone former: insufficient effect in idiopathic hypercalciuria.

The probability of being a stone former (PSF) was calculated in 3 groups of idiopathic calcium stone formers [with normocalciuria (NC), dietary hypercalciuria (DH) and idiopathic hypercalciuria (IH)] in 4 conditions: while on a free diet; on a calcium- and oxalate-restricted diet during 4 days; after an oxalate load, while on a 1.5-gram calcium diet, and after an oxalate load while on a calcium-restricted diet. Combined calcium and oxalate restriction significantly decreased PSF only in NC and DH whereas the decrease was not significant in IH because of a concomitant significant increase in oxalate excretion. Increase of PSF with the oxalate load was significantly greater during a calcium-restricted diet than during the 1.5-gram calcium diet in all groups of patients (4, 6 and 12 times greater in NC, DH and IH, respectively). These data show the critical role of oxalate restriction when calcium is restricted in order to decrease the PSF. This combined restriction is however not sufficient in idiopathic hypercalciuric patients to decrease their PSF.

Calcium↗
PubMed1985

[Medical treatment of idiopathic calcium lithiasis (I)].

Calcium stones is responsible for 80 per cent of the stones in the upper track. It is a frequent and particularly recurrent disease and for this reason it is important to prevent its recurrence by medical treatment, dissolution of calcium stones being impossible. In the first part of this review, we have presented the theoretical basis and the clinical studies concerning conservative therapy involving high fluid intake and dietary advice on calcium and oxalate intake. Then, for the various drugs proposed for recurrence prevention we have reviewed their mechanisms of action and the controlled clinical trials concerning these drugs. Finally, the practical therapeutical choices for the management of these patients are presented according to the results of the previous metabolic evaluation.

Calcium Oxalate↗
PubMed1984

Contractile activity of human coronary arteries and human myocardium in vitro and their sensitivity to calcium entry blockade by nifedipine.

Depolarization (100 mM K+) of acetylcholine, serotonin and prostaglandin (PG) F2 alpha contracted human isolated coronary artery segments. Serotonin was about 10-fold more potent than either acetylcholine or PGF2 alpha, but PGF2 alpha elicited contractions of the greatest magnitude. Serotonin (10 microM) and PGF2 alpha (3 microM) induced rhythmic contractions in the arterial segments. Depolarization-, PGF2 alpha- and serotonin-induced increase in tone was depressed by nifedipine, as was the serotonin- and PGF2 alpha -induced rhythmic activity. The induced rhythmic activity was about 100-fold more sensitive to inhibition by nifedipine than was the induced tonic contraction of the arteries. Depolarization-induced contractions and serotonin-induced rhythmic contractions displayed about equal sensitivity to inhibition by nifedipine. Nifedipine was more potent as an inhibitor of depolarization-induced contractions of arteries than it was as an inhibitor of electrically stimulated trabecular strips of ventricle from the same hearts. The inhibition of isolated coronary artery contraction was obtained within the range of nifedipine concentrations observed in the blood of treated patients.

Acetylcholine↗
PubMed1983

The inotropic effect of ouabain and its antagonism by dihydroouabain in rat isolated atria and ventricles in relation to specific binding sites.

The inotropic effect of ouabain has been studied in rat ventricles and atria. The concentration-effect curve of ouabain may be fitted by a model assuming the existence of two saturable components. The component with the higher sensitivity to ouabain accounted for 30% of the maximal increase in systolic tension in ventricles and for only 5% in atria. Increase in diastolic tension was only apparent at ouabain concentrations required to observe the low sensitivity component. [3H]-ouabain binding has been examined in microsomes prepared from atria and ventricles. High and low affinity binding sites have been observed. The ratio of high and low affinity ouabain binding sites was 4 fold lower in microsomes from rat atria than from rat ventricles. This could account for the difference in the response of these two tissues to the inotropic action of ouabain. In ventricular strips the high sensitivity component was much less apparent in the presence of dihydroouabain than with ouabain. When ventricular strips were preincubated in the presence of dihydroouabain 3 microM, the increase in systolic tension evoked by ouabain 1 microM was significantly reduced. Cumulative concentration-effect curve studies showed dihydroouabain antagonism to the high sensitivity component.

Animals↗