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Y Lecarpentier

Publications and source records attributed to Y Lecarpentier.

At least 145 records · Page 8Linked to original sources

Real-time kinetics of sarcomere relaxation by laser diffraction.

Kinetics of sarcomere movement were studied in real-time by laser diffraction. Instantaneous sarcomere shortening was measured during afterloaded twitches simultaneously with instantaneous shortening and tension of the whole trabecula excised from rat right ventricle. Resting sarcomere length at optimal length was 2.20 +/- 0.02 micron (mean +/- SEM). Maximum amplitude of sarcomere shortening was 0.30 +/- 0.01 and 0.16 +/- 0.01 micron, respectively, in twitches loaded with preload only, and in "isometric" twitches. When the isotonic load (expressed as a percentage of maximum isometric force TF) increased, the maximum velocity of sarcomere relaxation max Vr (micron/sec) decreased: max Vr = -4 exp (-2.5 X 10(-2) % TF); r = 0.95. The time course of sarcomere relaxation appeared to be progressively delayed when the total load increased from preload only up to "isometric" load. Sarcomere relaxation occurred in two successive exponential phases, a rapid phase [time constant (msec): tau 1] followed by a slower one (time constant: tau 2). When the total load increased, tau 1 increased and tau 2 decreased according to the linear relations: % TF = 0.2 tau 1 + 4.8 (r = 0.83) and % TF = -0.1 tau 2 + 157 (r = 0.95). The relative predominance of both the time course and the amplitude of these two phases depended upon the level of total load. The rapid process predominated at low load, the slow one at high load. The role of load and/or shortening in the time course of these two phases is discussed.

Animals↗

[In vitro opening of human atheromatous coronary arteries using a pulsed laser].

This study was undertaken to assess the respective values of pulsed and continuous laser emission for in vitro recanalisation of very stenosed atheromatous human coronary arteries. The Nd-YAG laser used emitted a 10 Hz 10 ns burst in the infrared band (1 064 microns). Previous spectroscopic studies had shown no specific band of absorption in the spectral field of emission of the usual lasers. The laser beam was focused in the axis of the segment of coronary artery irradiated. The crater or neo lumen obtained usually had irregular walls. No perforation of the arterial wall or macroscopic debris were observed. Histological studies showed minimal burn lesions with sparse coagulation necrosis limited to a few tens of micron thickness. The percentage recanalisation obtained with pulses of 200 mJ attained 50% for a total energy of 450 J delivered in 2 mn. This study confirmed the feasibility of disobliteration of atheromatous coronary arteries by pulsed laser. Our results suggest that ultra short pulsed laser acts more by a mechanical than by a thermal mechanism which may lead to less side effects than observed in vivo with continuous laser emission.

Coronary Disease↗

Load sensitivity of relaxation in the foetal and newborn rabbit heart.

Differences in the mechanism of cardiac relaxation and the influence of changes in the stimulation frequency were studied in foetal and newborn rabbit hearts. In the foetal rabbit heart which lacks a well developed sarcoplasmic reticulum, load sensitivity of relaxation was investigated and compared with that observed in the newborn. Load sensitivity was studied by measuring force and shortening length in twitches with increasing afterloads and also when load clamp steps were rapidly imposed during the twitch. Quantification of the load sensitivity was achieved by the measurement of the time to relaxation "tRi" which was linearly related to the relative developed force. The slope (S) of this linear relation quantifies the load sensitivity: the higher the slope, the more load sensitive is the relaxation. At a frequency of 24 beats X min-1, S was respectively 0.24 in the foetal heart and 0.36 in the newborn heart showing at both ages the existence of a load sensitivity and its significant increase at birth. No further increase in load sensitivity was observed from 1 day to 21 days after birth. Reducing the stimulation frequency from 24 to 10 beats X min-1 abolished the load sensitivity in foetal hearts (S = 0.05) while, in the newborn, a significant load sensitivity could still be observed (S = 0.25). Thus, in rabbit myocardium, the load sensitivity of cardiac relaxation depended upon the age and the stimulation frequency showing a perinatal development of the structures involved in the control of myocardial relaxation.

Animals↗

Relaxation of mammalian heart muscle during chronic cardiac overload.

Cardiac relaxation was studied in rat papillary muscle during hypertrophy induced by different chronic volume and/or pressure overload (aortic insufficiency, aorto-caval fistula, aortic stenosis, spontaneously hypertensive rat). Maximum velocity of lengthening did not depend upon the degree of cardiac hypertrophy, but rather on the type of chronic overload. Cardiac hypertrophy did not modify the load sensitivity of relaxation, whatever the type and stage of chronic overload, although, during acute hypoxia, the load sensitivity disappeared both in normal and in hypertrophied heart muscle.

Animals↗

Left ventricular isomyosins in normal and hypertrophied rat and human hearts.

Regulation of rat cardiac contractility by changes in the expression of a particular form of myosin (V1-V3) has been demonstrated with a pressure overload. Previous reports of the effect of a volume overload have been controversial. Therefore, we measured the isomyosin composition and mechanical function in the same papillary muscles from rat hearts subjected to a chronic volume overload (aortic insufficiency, AI). A marked change in isomyosin composition from V1 to V3 occurred. Contractility, as assessed by shortening velocity Vmax, was also significantly decreased, and this decrease was correlated with the isomyosin transformation. The changes in isomyosin composition and speed of contraction with AI are thus similar to changes induced by aortic stenosis. Little experimental evidence exists for involvement of such changes in the regulation of human cardiac contractility. Using immunoglobulins highly specific for V1 and V3 in autopsy samples we have observed that the human left ventricle is mostly composed of a V3 isoform (HV3) and that small amounts (1 to 15%) of a V1 type (HV1) are present in foetal and some adult hearts. This HV1 is absent from the left ventricles of patients with valvular disease, assessed at the time of valve replacement (N = 30, samples provided by Dr P. Menasché). Myosin Ca2+-stimulated ATPase activities were not significantly different between normal and hypertrophied hearts. These data demonstrate the heterogeneity of human ventricular myosin, which is composed of V1 and V3 isomyosins, as in other mammalian species. Isomyosin shifts from V1 to V3 are possible in man, but they are quantitatively small and without noticeable influence on overall ATPase activities.

Adenosine Triphosphatases↗

[Cardiac relaxation in experimental chronic myocardial hypertrophy: role of the sarcoplasmic reticulum].

The relaxation phase was studied in normal rat hearts submitted to chronic myocardial pressure and/or volume overload (stenosis of the abdominal aorta, aortic regurgitation, aorto-caval fistula) and in spontaneously hypertensive rats, some of which also had aorto-caval fistulae. Four indices were chosen to quantify the relaxation phase: maximal velocity of relaxation during contraction with preload alone, the negative peak of the derivative of isometric tension, and two other indices testing the sensitivity of the relaxation phase to other conditions of load. The first two indices were found to be depressed during chronic myocardial overload, especially with aorto-caval fistulae and mixed overload. On the other hand, the other two indices of the degree of sensitivity to the relaxation load by two different methods showed no significant difference between chronically overloaded and control hearts, though changes were observed after acute hypoxia. These two indices are related to morphological development and to the functional state of the sarcoplasmic reticulum. These results suggest that the rate of calcium uptake by the sarcoplasmic reticulum is reduced during chronic myocardial overload but that the myocardium retains its ability to regulate the relaxation phase with respect to time and the degree of total load. This property disappears temporarily after hypoxia when the heart behaves like frog myocardium which has practically no sarcoplasmic reticulum.

Animals↗

[The use of lasers in the study of cardiac mechanics].

Cardiac and skeletal muscles exhibit regularly spaced light and dark transverse striations (the I and A bands respectively). Consequently, when they are illuminated by a laser beam, they behave like diffraction gratings. The diffraction line spacing varies inversely with the sarcomere length. Real-time kinetics of sarcomere can be measured with a high accuracy. The analysis of the diffraction pattern indicates a high degree of synchronization of sarcomere movements (contraction and relaxation). This technique represents a powerful method to analyse the mechanical behaviour of heart muscle at subcellular level.

Humans↗

Spectral evidence for sub-picosecond iron displacement after ligand detachment from hemoproteins by femtosecond light pulses.

We have measured spectral and kinetic differences in protoheme, sperm whale or horse heart myoglobin and human hemoglobin following photodissociation induced by optical pulses of 80 fs duration. Full ligation was performed with oxygen or carbon monoxide. Femtosecond kinetics and transient difference spectra revealed the appearance of a deoxy species with tau approximately equal to 250-300 fs. The transient deoxy species in myoglobin and hemoglobin evidenced a 3-4 nm red shift of their delta A spectra compared with the equilibrium delta A spectrum. This shift was not observed after photodissociation of the carbon monoxide liganded protoheme. We proposed that the 250 fs time constant corresponding to the appearance of the deoxy-like species is related to the displacement of the ferrous iron out of the heme plane. Consequently, the small red shift of the delta A spectra observed in photodissociated hemoproteins may be tentatively attributed to changes in the vibrational modes of either the proximal histidine-Fe2+ bond and/or of the N4 porph-Fe-N epsilon His (F8) bent.

Animals↗

Force-velocity-length relationship during cardiac hypertrophy. Time course of activation.

Basic mechanical properties observed during cardiac hypertrophy were studied in left ventricular rat papillary muscles after exposure to chronic pressure and/or volume overloading. It is always possible, during such overloading conditions, to define the level of contractility in terms of a force-velocity-length (F-V-L) relationship regardless of time and initial length. Thus, during a determined period of the contraction phase and for a given total load, shortening velocity remained an univocal time-invariant function of shortening length, involving a time-independent maximum intensity of activation. The onset of this precise phase was reached relatively soon after stimulus. The time-independent F-V-L relation was observed both in controls and in hypertrophied heart muscles, whatever the degree and the type of induced hypertrophy, and even during the latest phases of congestive heart failure.

Animals↗

Femtosecond photolysis of CO-ligated protoheme and hemoproteins: appearance of deoxy species with a 350-fsec time constant.

Photolysis of HbCO, MbCO, and CO-protoheme has been investigated by measuring transient differential spectra and kinetics of induced absorption after excitation with a 250-fsec laser pulse at 307 nm. Probing was performed by a part of a continuum pulse between 395 and 445 nm. Photodissociation of the three liganded species occurred within the pulse duration. By contrast, the formation of deoxy species appeared with a mean (+/- SD) response time of 350 +/- 50 fsec. This time constant was identical for the three species and independent of the presence or absence of the protein structure. Our results suggest the formation of a transient high-spin in plane iron (II) species which relaxes in 350 fsec to a high-spin stable state with concerted kinetics of CO departure and iron displacement. The spin transition is suspected to occur via liganded excited states which relax in part to non-reactive states with a 3.2-psec time constant.

Carbon Monoxide↗

Load dependence of mammalian heart relaxation during cardiac hypertrophy and heart failure.

Mechanical properties of relaxation were studied in left ventricular rat papillary muscle during cardiac hypertrophy induced by chronic pressure and/or volume overload. Maximum velocity of isotonic lengthening was linearly related to total extent of isotonic shortening and to maximum velocity of isotonic contraction and depended on the type of chronic overloading without correlation with the degree of cardiac hypertrophy. Time to peak shortening was significantly increased in each group of hypertrophied heart muscles as compared to controls. The sensitivity of cardiac relaxation to the loading conditions was determined by the time course of relaxation. To quantify the degree of load sensitivity, we measured the ratio of isotonic area to isometric area, which was the area limited by the afterloaded force vs. time at 50% of the isometric peak tension divided by the area of the force vs. time trace in the isometric twitch below the same level of load. The value of this ratio was about 0.81 in normal rat and did not show any significant differences in hypertrophied heart muscles even at the terminal stage of congestive heart failure. During acute hypoxia the load sensitivity of relaxation disappeared both in normal and in hypertrophied hearts. Thus inadequacy in oxygen supply has more drastic effects, as compared with those induced by chronic overload, probably by affecting the sarcoplasmic reticulum uptake of activating calcium.

Animals↗

Post-extrasystolic left ventricular peak pressure with and without left ventricular failure.

18 patients without valvular pathology, coronary artery disease, or idiopathic hypertrophic subaortic stenosis were haemodynamically and angiographically investigated in order to analyse the effects of a ventricular extrasystolic beat upon the post-extrasystolic left ventricular peak pressure. In eight normal patients (group I), the post-extrasystolic peak pressure (P.ES.P.P.) was lower than that of the pre-extrasystolic beat; in 10 patients with symptoms of left ventricular failure (group II) the P.ES.P.P. significantly increased. The reasons are: 1) cardiac origin: stroke volume increased more in group II; 2) arterial origin. a) aortic compliance was lower in group II (this is probably related to the older age of patients in group II), and by decrease in end-diastolic aortic pressure was smaller in group II. Part of this arterial effect (2b) may probably be explained from the fact that post-extrasystolic compensatory pauses are equal in both groups, but the decay time of arterial pressure during diastole (assuming an exponential decay) is larger in group II. At the same age and with the identical aortic compliance only the two factors 1 and 2b play a part in the changes in P.ES.P.P.

Adult↗