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Biomedical subjects

Y Lecarpentier

Publications and source records attributed to Y Lecarpentier.

At least 127 records · Page 7Linked to original sources
PubMed1990

Inotropic and lusitropic effects of chlorpromazine on rat left ventricular papillary muscle.

The in vitro effects of chlorpromazine on rat cardiac papillary muscle were tested at 10(-6), 10(-5) and 10(-4) M. Mechanical parameters were determined from the contraction and relaxation phases under isotonic and isometric conditions in order to assess contraction, relaxation, contraction-relaxation coupling and load sensitivity of relaxation. The peak power output Emax was determined from the force-velocity relationship. At 10(-6) M, a slight positive inotropic effect was observed, probably related to modifications in cross-bridges kinetics. Negative inotropic effects were observed with 10(-5) and 10(-4) M chlorpromazine. At 10(-5) M, shortening of the isometric relaxation and decrease in R2 = (+dF.dt-1max)/(-dF.dt-1max) suggest that chlorpromazine also diminishes myofilament Ca++ sensitivity. Emax was increased at 10(-6) M (19 +/- 5%, P less than .05), but decreased at 10(-5) M (-28 +/- 10%, P less than .05) and 10(-4) M (-82 +/- 2%, P less than .05). Modifications in the force-velocity relationship at 10(-4) M indicated that lowering myocardial performance by chlorpromazine was associated with a low muscle efficiency from a thermoenergetic point of view. At all concentrations, chlorpromazine impaired the isotonic relaxation and load sensitivity of relaxation. At 10(-4) M, muscle contracture and slowed isometric relaxation were probably due to "calcium overload." These results showed that chlorpromazine finely modulates intrinsic cardiac energetics and mechanics by acting on the sarcoplasmic reticulum, myofilament Ca++ sensitivity and cross-bridges kinetics, according to the level of load and chlorpromazine concentration used.

Animals↗
PubMed1989

Diazepam does not improve the mechanical performance of rat cardiac papillary muscle exposed to chloroquine in vitro.

Diazepam has been reported to decrease the cardiac toxicity of chloroquine but the precise mechanism involved remains unknown. Left ventricular papillary muscles from adult Wistar rats were exposed to 10(-4) M chloroquine and assigned to three groups: group I (n = 10) exposed to chloroquine alone; group II (n = 8) exposed to chloroquine and 10(-5) M diazepam; group III (n = 8) exposed to chloroquine and 10(-4) M diazepam. The main mechanical parameters measured were: maximum unloaded shortening velocity (Vmax), maximum lengthening velocity (maxVr), active force normalized per cross-sectional area (AF/s), contraction-relaxation coupling under low load (R1), load sensitivity of relaxation (Isot.A/Isom.A), and peak power output (Emax) determined from Hill's equation of the force-velocity curve. Data are expressed as mean percent of control values +/- SD, for groups I, II, III respectively. No differences between groups I, II, and III were noted for Vmax (87 +/- 13, 82 +/- 9, 86 +/- 7), maxVr (47 +/- 6, 48 +/- 11, 52 +/- 11), AF/s (87 +/- 16, 91 +/- 10, 83 +/- 11), Isot. A/Isom. A (113 +/- 9, 108 +/- 3, 109 +/- 7), or Emax (75 +/- 10, 81 +/- 12, 72 +/- 16). Chloroquine was shown to be a negative inotropic agent since it decreased Vmax, AF/s and Emax, but diazepam did not restore the intrinsic mechanical performance of rat cardiac papillary muscle exposed to chloroquine, therefore 1) the protective cardiovascular effects of diazepam in chloroquine poisoning are not related to an improvement in intrinsic cardiac mechanical properties; 2) inotropic agents are therefore necessary in combination with diazepam for the treatment of severe chloroquine poisoning.

Animals↗
PubMed1989

Lusitropic effect and modifications of contraction-relaxation coupling induced by alpha-adrenergic stimulation in rat left ventricular papillary muscle.

Phenylephrine (PE) and metaraminol (MR) were studied alone at 2 x 10(-5) M and at 4 x 10(-5) M respectively. These drugs were also used both in the presence of either propranolol (PR) at 4 x 10(-7) M (PE/PR and MR/PR groups) or prazosin (PZ) at 2 x 10(-7) M (PE/PZ and MR/PZ groups). Specific alpha-adrenergic stimulation (AS) was induced in the PE/PR and MR/PR groups. These AS were evaluated in isotonic and isometric conditions on rat left ventricular papillary muscle. Peak shortening velocity (Vcmax) and peak lengthening velocity (Vrmax) were calculated from the twitch with preload only. Positive (+dF/dtmax) and negative (-dF/dtmax) peak derivative forces were calculated from the isometric twitch. Two coefficients R1 and R2 were used to measure the coupling between contraction and relaxation at low and heavy load, respectively: R1 = Vcmax/Vrmax and R2 = (+dF/dtmax)/(-dF/dtmax). In all groups, there was a significant positive inotropic effect. As compared to control values before AS, R1 significantly decreased in all groups, (PE/PR: -15%; MR/PR: -18%; PE/PZ: -8%; MR/PZ: -23%; PE: -19%; MR: -32%). On the other hand, R2 significantly decreased only in three groups (PE/PZ: -5.4%; MR/PZ: -16.5%; MR: -12.0%) whereas it did not significantly change in the three other groups (PE/PR; MR/PR; PE). In all groups, and at low load, Vrmax increased more than Vcmax (positive relaxant effect i.e. R1 decreased). At heavy load, despite the positive inotropic effect, there was no significant relaxant effect after predominent alpha-AS. These results indicate that alpha-AS modified the coupling between contraction and relaxation differently, depending on the level of load.

Adrenergic alpha-Agonists↗
PubMed1989

Inotropic effect of ketamine on rat cardiac papillary muscle.

The direct effect of ketamine on cardiac muscle was studied using rat left ventricular papillary muscle. At an extracellular calcium concentration [( Ca++]0) of 2.5 mM, rat myocardial contractility is nearly maximum, and a positive inotropic effect was demonstrated by an increase in maximum shortening velocity (Vmax) with ketamine at 10(-5) M but not 10(-4) M. At a [Ca++]0 of 0.5 mM, ketamine 10(-5) and 10(-4) M had a positive inotropic effect as shown by an increase in Vmax (135% +/- 22% and 147% +/- 33%, respectively) and in isometric active force (AF/s) (120% +/- 10% and 152% +/- 44%, respectively). The positive inotropic effect of ketamine was not related to catecholamine uptake inhibition and/or alpha/beta receptor stimulation because it persisted after phentolamine and propranolol and because ketamine had no relaxing effect. Ketamine 10(-5) and 10(-4) M impaired isotonic relaxation, contraction-relaxation coupling under low loading conditions, and the load sensitivity of relaxation, which suggests impairment of the calcium sequestering systems, especially the sarcoplasmic reticulum (SR). Ketamine modified postrest recovery: the first beat (B1) after a 1-min rest period was decreased by ketamine 10(-4) M but not ketamine 10(-5) M. Moreover, the beat-to-beat postrest recovery has been demonstrated to be exponential, and tau, the time constant of the decay was increased by ketamine 10(-4) M (5.4 +/- 0.3 vs. 3.9 +/- 0.2 beats) but not by ketamine 10(-5) M (3.4 +/- 0.4 vs. 3.7 +/- 0.2 beats). These effects on postrest recovery suggest that ketamine impairs SR function. The authors suggest that ketamine had a dual action on rat myocardium: a positive inotropic effect without any relaxing effect, probably related to an increase in calcium influx, and an impairment of SR function. Nevertheless, impairment of SR is only significant at high concentration (10(-4) M) and might overcome the positive inotropic effect only at supratherapeutic concentration.

Animals↗
PubMed1989

[Pulsed lasers in the treatment of urinary calculi].

Intracorporeal lithotripsy of urinary calculi by pulsed dye laser recently enriched the urologist's therapeutic arsenal. We recall the in vitro studies and animal experimentations which demonstrated the feasibility of laser lithotripsy and the absence of harmful tissue damage. The ideal indications for intracorporeal lithotripsy are ureteral stones accessible by rigid and, more especially, flexible ureteroscopy. The results of the first published series using this technique are very encouraging.

Animals↗
PubMed1989

[Endocorporeal lithotripsy using a pulsed laser].

Intracorporeal lithotripsy of urinary calculi by pulsed dye laser has recently enriched the urologist's therapeutic arsenal. We recall the in vitro studies and animal experimentations which demonstrated the feasibility of laser lithotripsy and the absence of harmful tissue damage. The ideal indications for intracorporeal lithotripsy are ureteral stones accessible by rigid and, more especially, flexible ureteroscopy. The results of the first published series using this technique are very encouraging.

Humans↗
PubMed1988

Relaxation of the diaphragm muscle: influence of ryanodine and fatigue.

Relaxation of rat diaphragm was shown to be sensitive to load, as previously described for adult mammalian ventricular muscle, because the time course of isotonic relaxation could be changed by changing the load: the lighter the load, the greater the shortening, the quicker the relaxation. Maximum velocity of isotonic relaxation was linearly related to the extent of shortening (r = 0.90). To quantify the degree of load sensitivity, we measured the tRi, i.e., the ratio of time at which the isometric relaxation of the twitch afterloaded at 50% of the isometric peak active tension began to time at which the isometric twitch was relaxed to 50% of the isometric peak active twitch tension. tRi was 0.76 +/- 0.03 (SE) in control conditions but significantly increased to 0.91 +/- 0.02 after ryanodine, which is an inhibitor of the sarcoplasmic reticulum (SR) function, and to 0.89 +/- 0.03 after fatigue. These results suggest that in adult rat diaphragm, as in cardiac muscle, the load sensitivity of relaxation requires a well-functioning SR and that the relaxation abnormalities observed in fatigued diaphragm are related to a dysfunction of the SR.

Alkaloids↗
PubMed1987

Coordinated changes in contractility, energetics, and isomyosins after aortic stenosis.

To investigate possible alterations of myocardial performance in young rats, cardiac hypertrophy was induced by stenosis of the ascending aorta (AS) in three groups of 25-day-old rats that were compared with three groups of sham-operated controls (C). The cardiac overload duration was 8-10 days, 1 mo, and 2 mo in groups 1, 2, and 3, respectively. Mechanics and energetics were studied in left ventricular papillary muscles, and determination of the V1 and V3 isomyosin pattern was achieved in the same papillary muscle. The majority of quantitative changes concerning the cardiac growth process, contractility, and isomyosin shifts occurred within 8-10 days of stenosis. At this point, the degree of left ventricular hypertrophy relative to C was 53 +/- 6%, whereas maximum unloaded shortening velocity (Vmax) decreased significantly (2.8 +/- 0.1 in C vs. 1.9 +/- 0.1 Lmax/s in AS), peak power output (Emax) decreased (1.8 +/- 0.3 in C vs. 0.6 +/- 0.1 in AS), and the curvature of Hill's hyperbola increased (1.3 +/- 0.4 in C vs. 2.0 +/- 0.7 in AS); moreover, the percent V1 isomyosin decreased significantly (98 +/- 1 in C vs. 51 +/- 3% in AS) and the percent V3 isomyosin increased significantly (2 +/- 1 in C vs. 26 +/- 2% in AS). Beyond 8-10 days of AS, additional changes in cardiac hypertrophy and in mechanical and biochemical parameters were less marked.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Changes in LV papillary muscle performance and myosin composition with aortic insufficiency in rats.

Aortic insufficiency was induced in rats. Left ventricular papillary muscle function was studied after 5, 12, and 40 wk and compared with the papillary muscles from sham-operated animals. The maximum unloaded velocity of shortening, Vmax, was decreased in the rats with aortic insufficiency relative to controls by 15, 20, and 34% at 5, 12, and 40 wk, respectively. The decrease in Vmax occurred concomitantly with a change in the myosin isoenzyme composition such that the V1 isoform content decreased and the V3 isoform increased. Relative to age-matched controls, the V3 content in the hearts with aortic insufficiency had increased by 80, 180, and 125% at 5, 12, and 40 wk, respectively. The decrease in Vmax in the aortic insufficiency group muscles correlated with the change in myosin isozyme composition and could not be explained by changes in collagen content. Thus aortic insufficiency induced changes in myosin isozyme content and Vmax similar to those previously observed with aortic stenosis, thus suggesting a common mechanism of myocardial adaptation to different types of mechanical overload.

Animals↗
PubMed1987

Major alterations in relaxation during cardiac hypertrophy induced by aortic stenosis in guinea pig.

Left ventricular hypertrophy (LVH) was produced in guinea pigs after aortic stenosis (AS). The percentage of LVH in AS was determined by normalizing left ventricular (LV) weight by the mean LV weight of sham-operated controls (n = 12). After 3 weeks of cardiac overload, a mild LVH (30 +/- 3%) was induced in 17 animals and a relatively severe LVH (56 +/- 3%) was induced in 7 animals. LV papillary muscles were rapidly excised for mechanical studies. No significant differences were observed between control and mild hypertrophy groups. In contrast, a marked decrease in myocardial performance was seen in the more severe cardiac hypertrophy group and was expressed as a percentage of sham-operated levels (Vmax, 22%; active isometric force/mm2, 23%; +dF/dt max/mm2, 26%). Relaxation in this group was still more impaired than contraction (peak lengthening velocity, 14%; -dF/dt max/mm2, 19%). Moreover, the load sensitivity of relaxation was present in both sham-operated controls and mild hypertrophy but almost disappeared in more severe hypertrophy. Isometric relaxation was delayed in the latter group, as shown by the 15% increase of the half-time of the decline of isometric relaxation (t 1/2). On the other hand, acute hypoxia (95% N2-5% CO2 for 20 minutes) also induced a fall in contractility and the disappearance of the load sensitivity of relaxation but with a 67% decrease of t 1/2. Thus, the mechanical analysis of relaxation allows the effects of chronic overload in relatively severe cardiac hypertrophy to be separated from those of acute hypoxia. Moreover, in severe cardiac hypertrophy, the impairment of the load sensitivity of relaxation with increased t 1/2 strongly suggests alterations of the sarcoplasmic reticulum, especially since the moderate decrease in the myofibrillar ATPase activity, which has been observed previously in guinea pig pressure overload, cannot account completely for the marked fall in myocardial performance.

Adenosine Triphosphatases↗
PubMed1987

[Influence of preload on myocardial relaxation in the rat].

Preload, which determines the initial muscle length, has proved to be a basic determinant of the muscle relaxation phase. The mechanical properties of the papillary muscle of Wistar rats (n = 20) were studied at different initial lengths (L): Lmax and 98 p. 100, 94 p. 100, 90 p. 100, 86 p. 100 and 82 p. 100 Lmax. In isometry, the relaxation phase was proportionally less sensitive to a reduction of preload than the contraction phase. When L decreased the peaks of maximal force derivative of the contraction phase (+dF.dt-1 max) and relaxation phase (-dF.dt-1 max) were linearly and significantly lowered at L = 94 p. 100 Lmax and L = 90 p. 100 Lmax respectively. Conversely, in isotonia the relaxation phase was much more sensitive to a reduction of preload than the contraction phase. On a muscle preloaded from 82 p. 100 Lmax to Lmax, the highest max Vr value (i.e. maximal speed of isotonic relaxation) was measured at Lmax, which is the apex of the Starling's isometric curve. When L decreased max Vr decreased linearly and significantly at 94 p. 100 Lmax. In contrast, the maximal speed of contraction (max Vc) increased between Lmax and 94 p. 100 Lmax, became maximal, then significantly decreased beyond 82 p. 100 Lmax. Thus, in the physiological range of the myocardium (Lmax - 85 p. 100 Lmax) the rat papillary muscle tended to maintain its maximal isotonic speed of contraction, or even to increase that speed, whereas the isometric contraction, isometric relaxation and isotonic relaxation phases were early and significantly depressed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Relationship between inotropy and relaxation in rat myocardium.

Myocardial mechanics of 56 rat papillary muscles were investigated in various inotropic states, i.e., early postpartum (1st day, 1st mo) and, in adult, by altering external calcium concentration, [Ca2+]0, stimulation frequency (F), and initial muscle length (L). In all these protocols, the decrease of the inotropic level paralleled a progressive diminution in load sensitivity of relaxation. In such protocols modifying cardiac contractility, peak shortening velocity of the twitch with preload only at Lmax (Vcmax) was always less depressed than peak lengthening velocity (Vrmax), and the ratio R1 = Vcmax/Vrmax always increased. This increase of R1 was linearly related with the decrease of the maximum unloaded shortening velocity (Vmax). The ratio R2 (positive over negative peak force derivatives of the isometric twich at Lmax) was significantly lowered in newborn and was lowered in adult for [Ca2+]0 less than or equal to 1 mM and L less than or equal to 94% Lmax. For a given change in Vmax, each of the experimental protocols gave rise to specific changes in contraction-relaxation coupling tested at low load (R1) and at heavy load (R2).

Aging↗
PubMed1986

[The mechanics of sarcomeres studied using laser diffraction. A study of relaxation].

Myocardial tissues act as an optical filter to light. This is due to their regular striation--periodically alternating clear and dark anisotropic bands. When a narrow band of rat right ventricle is illuminated with a Helium-Neon laser (lambda = 633 nm) diffraction bands are observed, the spacing of which is inversely proportional to the sarcomere length. After muscular stimulation, the displacement of the diffraction bands allows measurement in real time of the contraction and relaxation of the sarcomeres. Sarcomere relaxation comprises two successive experimental phases, one rapid and the other one slow. The time constant of the rapid phase (tau 1) increases linearly with the total load; that of the slow phase (tau 2) decreases. The end of the rapid phase and tau 1 depend on the conditions of load. Our results suggest that the recaptation of calcium by the sarcoplasma reticulum and the affinity of troponine C for calcium depend on the level and changes of load. The affinity of TnC for calcium increases with high load and/or low amplitude of sarcomere shortening: it decreases with low loads and/or high amplitudes of sarcomere shortening.

Animals↗