Biomedical subjects

Y Lecarpentier

Publications and source records attributed to Y Lecarpentier.

At least 73 records · Page 4Linked to original sources

PubMed1996

Myocardial effects of eltanolone in hamsters with hypertrophic cardiomyopathy.

Eltanolone is a new short-acting i.v. induction agent that induces less cardiovascular depression than propofol or thiopentone and has no significant effect on intrinsic contractility in normal myocardium. However, its effects on diseased myocardium are unknown. We have studied in vitro the effects of eltanolone 0.1, 1, and 10 micrograms ml-1 on the intrinsic contractility of left ventricular papillary muscles from normal hamsters and those with hypertrophic cardiomyopathy (strain BIO 14.6, 6-month-old) (Krebs-Henseleit solution, 29 degrees C, pH 7.40, Ca2+ 2.5 mmol litre-1, stimulation frequency 3 min-1). Cardiac hypertrophy (mean 134 (SD 9)%, P < 0.001) was observed in cardiomyopathic hamsters. Contractility of papillary muscles from hamsters with cardiomyopathy was less than that of controls, as shown by the lower active isometric force (8 (3) vs 35 (14) mN mm-2, P < 0.001). Eltanolone did not induce any significant inotropic or lusitropic effects in normal hamsters, and the effects of eltanolone were not significantly different between normal hamsters and those with cardiomyopathy.

Anesthetics, Intravenous↗

PubMed1996

Blood flow acceleration in the carotid and brachial arteries of healthy volunteers: respective contributions of cardiac performance and local resistance.

The influence of local resistance and cardiac performance on peripheral blood acceleration was investigated in 14 healthy male volunteers. Steady and pulsatile flow was studied in the brachial and in the common carotid arteries, ie, two territories that exhibit marked differences in resistive characteristics. Instantaneous blood velocity (V), mean blood velocity (Vm) and artery diameter (D) were evaluated at rest by an ultrasonic range-gated pulsed Doppler flowmeter using a double transducer probe, thus allowing the calculation of mean blood flow (Q). Mean local resistance (R) was obtained by dividing the mean arterial pressure by Q. The peak value of the local acceleration of the blood was obtained by computer-assisted calculation of the first derivative of instantaneous blood velocity (Gmax = +dV/dtmax). Peak aortic blood acceleration (GAo) was simultaneously measured from the suprasternal notch using a pulsed Doppler velocity meter. In the branchial and the common carotid arteries, Gmax was of a similar magnitude (551 +/- 30 and 555 +/- 44 cm/s2, respectively) despite major differences in the respective D, Vm, Q and R values. In neither artery was there a relationship between Gmax and either resting Q or R. At the brachial artery level, Gmax was positively related to GAo (r = 0.79, P = 0.0008). At the common carotid artery level, there was a weak, although non significant relationship between Gmax and GAo (P = 0.08). Our results indicate that the local acceleration of peripheral blood flow in the brachial artery is related rather to upstream central impulse than to downstream hemodynamics, and suggest some regional differences in the hemodynamic determinants of the local acceleration of peripheral blood flow.

Adult↗

PubMed1996

Matching dicrotic notch and mean pulmonary artery pressures: implications for effective arterial elastance.

It has been suggested that pulmonary artery pressure at the end of ejection is close to mean pulmonary artery pressure, thus contributing to the optimization of external power from the right ventricle. We tested the hypothesis that dicrotic notch and mean pulmonary artery pressures could be of similar magnitude in 15 men (50 +/- 12 yr) referred to our laboratory for diagnostic right and left heart catheterization. Beat-to-beat relationships between dicrotic notch and mean pulmonary artery pressures were studied 1) at rest over 10 consecutive beats and 2) in 5 patients during the Valsalva maneuver (178 beats studied). At rest, there was no difference between dicrotic notch and mean pulmonary artery pressures (21.8 +/- 12.0 vs. 21.9 +/- 11.1 mmHg). There was a strong linear relationship between dicrotic notch and mean pressures 1) over the 10 consecutive beats studied in each patient (mean r = 0.93), 2) over the 150 resting beats (r = 0.99), and 3) during the Valsalva maneuver in each patient (r = 0.98-0.99) and in the overall beats (r = 0.99). The difference between dicrotic notch and mean pressures was -0.1 +/- 1.7 mmHg at rest and -1.5 +/- 2.3 mmHg during the Valsalva maneuver. Substitution of the mean pulmonary artery pressure by the dicrotic notch pressure in the standard formula of the pulmonary vascular resistance (PVR) resulted in an equation relating linearly end-systolic pressure and stroke volume. The slope of this relation had the dimension of a volume elastance (in mmHg/ml), a simple estimate of volume elastance being obtained as 1.06(PVR/T), where T is duration of the cardiac cycle. In conclusion, dicrotic notch pressure was of similar magnitude as mean pulmonary artery pressure. These results confirmed our primary hypothesis and indicated that human pulmonary artery can be treated as if it is an elastic chamber with a volume elastance of 1.06(PVR/T).

Blood Pressure↗

PubMed1996

Sarcomere relaxation in hamster diaphragm muscle.

We characterized instantaneous sarcomere relaxation over the load continuum in isolated hamster diaphragm muscles by means of laser diffraction. In afterloaded twitches, sarcomere relaxation displayed two consecutive phases. The bulk of sarcomere lengthening occurred during the first phase and corresponded in time to muscle lengthening. The second phase of sarcomere relaxation was slower and corresponded in time to tension decay. At initial muscle length, the peak velocity of sarcomere lengthening (SVL) was linearly related to both the maximum extent of sarcomere shortening (delta SL) and sarcomere length at peak shortening (SLmin; each P < 0.01). Varying preload modified the SVL vs. SLmin relationship but not the SVL vs. delta SL relationship. At a given preload, muscle tension decay began at a similar sarcomere length, regardless of the afterload level. In conclusion, our results support the role played by sarcomere length in regulating the diaphragm muscle-lengthening rate but not the rate of tension decline.

Animals↗

PubMed1996

Mechanical and energetic effects of cromakalim on guinea pig left ventricular papillary muscle.

The mechanical and energetic effects of the adenosine triphosphate-sensitive potassium channel opener cromakalim at 50 microM and 100 microM were determined on guinea pig left ventricular papillary muscles and compared with those of low calcium concentration (n = 9 in each group). Both concentrations of cromakalim induced a negative inotropic effect (decrease in maximum shortening velocity at preload only and maximum extent of muscle shortening at preload only, P < .01 and P < .001 at 50 and 100 microM, respectively; maximum isometric active force normalized per cross-sectional area during the isometric twitch, P < .001; positive peak of the isometric force derivative normalized per cross-sectional area, P < .001) and a negative lusitropic effect (decrease in maximum lengthening velocity at preload only and negative peak of the isometric force derivative normalized per cross-sectional area, P < .01 and P < .001 at 50 and 100 microM, respectively). At 100 microM, the decrease in relaxation parameters was more marked than that in contraction parameters under isotonic conditions, as shown by the decrease in the slope of the relationship between peak lengthening velocity and maximum extent of muscle shortening (P < .01); this result reflects an intrinsic negative relaxant effect. No relaxant effect was found under isometric conditions at either concentration. The mechanical effects of low calcium were similar to those of cromakalim 100 microM, which suggests that the drug acted mainly by reducing the cellular calcium entry. Despite the negative mechanical effect of cromakalim, mechanical efficiency was preserved. This could partly explain the cardioprotective effect of cromakalim during ischemia.

Action Potentials↗

PubMed1996

[Relationship between end-systolic aortic pressure and mean aortic pressure in adults].

The mean blood pressure is an accurate estimate of the end-systolic aortic pressure in children. The aim of this study was: 1) to assess the relationship between the pressure at the incisura (PIAo) and the mean (MAoP) and pulse (PAoP) pressures of the supravalvular aorta in adults: and 2) to evaluate MAoP as an estimate of PIAo in adults. High fidelity pressure recordings were carried out in the supravalvular aorta in 17 men. The pressures were measured at rest in 10 consecutive beats and. In 6 subjects, during a Valsalva manoeuvre. At rest, PIAo was greater than the MAoP (109 +/- 17.9 versus 99.6 +/- 12.5 mmHg, p = 0.0001). There was a positive linear correlation between PIAo and MAoP (r = 0.93) and between PIAo and PAoP (r' = 0.77) whereas no correlation was observed between PIAo and heart rate, cardiac output or estimated total systemic arterial compliance. A beat-to-beat relationship was observed between PIAo and MAOP: 1) at rest in 16 of the 17 subjects and 2) in each subject who performed a Valsalva manoeuvre. Both at rest and during Valsalva, MAOP underestimated PIAo significantly, especially when PIAo was increased (p = 0.0001). The authors conclude that end-systolic supraaortic pressure is mainly related to the mean component of aortic pressure. MAOP slightly but constantly underestimated PIAo and this should lead to caution in assimilating MAOP to end-systolic aortic pressure in adults, especially in subjects with very high aortic pressures.

Adult↗

PubMed1995

Relation between aortic dicrotic notch pressure and mean aortic pressure in adults.

It has recently been suggested that mean arterial pressure provides a reliable estimate of dicrotic notch pressure in infants and children. The aim of the present study was twofold: (1) to investigate the relation existing between aortic dicrotic notch pressure and both the steady and pulsed component of aortic pressure in adults (i.e., mean and pulse aortic pressures, respectively); and (2) to evaluate mean aortic pressure as an estimate of aortic dicrotic notch pressure. High-fidelity pressure recordings were obtained at the aortic root level in 17 men (52 +/- 13 years). Pressure data were analyzed at rest over 10 consecutive beats in each patient, and, in 6 patients, during the Valsalva maneuver (over 22 to 50 consecutive beats). At rest, dicrotic notch pressure was greater than mean pressure (109.0 +/- 17.9 vs 99.6 +/- 12.5 mm Hg, p = 0.0001). Dicrotic notch pressure was positively related to mean pressure (r = 0.93) and to pulse pressure (r' = 0.77), but not to patient's heart rate, cardiac output, or total estimated arterial compliance. There was a spontaneous beat-to-beat relation between dicrotic notch and mean pressures (1) at rest in 16 of 17 patients (mean r = 0.85), and (2) in all patients undergoing the Valsalva maneuver (mean r = 0.97). During the maneuver, intravascular mean pressure ranged from 59 to 171 mm Hg. Dicrotic notch pressure was positively related to mean pressure (r = 0.98) and to pulse pressure (r' = 0.44). Both at rest and during the Valsalva maneuver, mean pressure underestimated dicrotic notch pressure, and the higher the dicrotic notch pressure, the more negative the percent error (each p = 0.0001). In conclusion, aortic dicrotic notch pressure was mainly related to the steady component of aortic pressure. The mean aortic pressure slightly but significantly underestimated aortic dicrotic notch pressure, and thus should be used with greater caution in adults than in young patients as an estimate of end-systolic pressure.

Adult↗

PubMed1995

Influence of dietary polyunsaturated fatty acids on contractility, lusitropy and compliance of isolated rat myocardium.

Two groups of 15 rats were fed for 4 weeks with diets containing 15% by weight of fat varying in polyunsaturated fatty acids (PUFA) content and type. Diet C18:2 (n-6) contained 20% of total fatty acids as linoleic acid and small amount of (n-3) PUFA (0.4% of the total fatty acids). Diet LC (n-3) contained the same amount of 18:2 (n-6) and of long chain (n-3) C20 and C22 PUFA (10% of the total fatty acids). Contents of both saturated fatty acids and amount of total PUFA were kept constant in the two diets. Left ventricular papillary muscle mechanics were studied blind at Lmax and over the entire load-continuum, in terms of inotropy, characteristics of the force-velocity relationship, relaxation and compliance. Inotropy, force-velocity relationships and muscle compliance were similar in both groups. There was a trend towards a lower peak lengthening velocity at preload in the LC (n-3) group (P = 0.10) together with an unchanged peak rate of isometric force decline. This resulted in a significant impairment of the two mechanical indexes testing the load dependence of myocardial relaxation (P = 0.019 and P = 0.002). In conclusion, short-term differences in PUFA regimen were associated with an unchanged myocardial contractility and economy of force generation. The decreased load dependence of relaxation together with unchanged myocardial compliance strongly favored a physiological relevance of the previously reported modifications of sarcoplasmic reticulum phospholipid composition and calcium transport under (n-3) PUFA regimen.

Animals↗

PubMed1995

Left ventricular diastolic function in asymptomatic and symptomatic human immunodeficiency virus carriers: an echocardiographic study.

Acquired immunodeficiency syndrome (AIDS) is a systemic illness affecting multiple organs, including the heart. Left ventricular (LV) diastolic dysfunction has been reported as the first echocardiographically detectable abnormality in several cardiovascular disorders. We tested the hypothesis that Human Immunodeficiency Virus (HIV) carriers have LV diastolic impairment when studied early in the clinical course of the infection. Doppler echocardiographic and computerized time-motion parameters of LV diastolic function were obtained in 51 HIV patients and in 25 age- and sex-matched healthy controls. The HIV population consisted of 28 totally asymptomatic subjects and 23 patients with incipient AIDS. As compared to controls, the HIV group had similar heart rate, blood pressure level, LV dimensions and fractional shortening, but increased isovolumetric relaxation time (P = 0.03), early filling duration (P < 0.001) and decreased early mitral flow peak velocity (E) (P = 0.02) and EF slope (P < 0.001). HIV patients also showed lower values for posterior wall thinning (PWT, P < 0.01) and peak lengthening velocity of the posterior wall (PVL, P < 0.05), and a trend to a decreased peak rate of LV enlargement in diastole (D+, P = 0.05). Doppler-derived parameters of diastolic function were significantly altered in the asymptomatic HIV group vs controls. The LV diastolic indices were similar in symptomatic and asymptomatic HIV patients except for PWT, which was lower in the symptomatic HIV group (P = 0.04). Since mild and focal wall motion abnormalities were detected in 11 HIV carriers (22%), comparison of LV diastolic indexes between HIV patients and controls was also performed in two subgroups; these included asymptomatic (n = 26) and symptomatic (n = 14) patients with normal contractile state. The two subgroups had abnormalities of diastolic function similar to those of the HIV group as a whole, but with somewhat lower levels of statistical significance. Our data strongly suggest that there is myocardial involvement at the early stage of HIV infection; however, its impact on the clinical course of the disease remains to be clarified.

Acquired Immunodeficiency Syndrome↗

PubMed1995

Dipyridamole slows the rate of isovolumic pressure fall in patients with normal coronary arteries.

Dipyridamole is currently used for thallium imaging and stress echocardiography. The coronary and haemodynamic effects of dipyridamole are well documented while its effects on left ventricular relaxation remain to be determined. The aim of the present study was to evaluate the effects of dipyridamole on left ventricular relaxation rate in healthy subjects. High fidelity pressure recordings were obtained at fixed atrial pacing (89 +/- 2 beats.min-1) in 10 subjects with normal left ventricular angiography and coronary arteriograms. Left ventricular pressure was recorded at rest and 5 min after a 4 min infusion of dipyridamole (0.14 mg.kg-1.min-1). Dipyridamole infusion decreased left ventricular systolic pressure (P < 0.01) and time to left ventricular systolic pressure (P < 0.01), with no changes in end-diastolic pressure or peak rate of pressure rise. The peak rate of isovolumic pressure fall decreased (from 1957 +/- 105 to 1488 +/- 100 mmHg.s-1, P < 0.01) and the time constant of isovolumic relaxation increased (from 37 +/- 2 to 44 +/- 3 ms, P < 0.02). In conclusion, our study indicates that acute administration of clinically relevant doses of dipyridamole displays deleterious effects on heart relaxation in healthy humans.

Arteries↗

PubMed1995

Myocardial effects of propofol in hamsters with hypertrophic cardiomyopathy.

BACKGROUND: Propofol is a short-acting intravenous induction agent that induces cardiovascular depression but without significant effect on intrinsic myocardial contractility in various species. However, its effects on diseased myocardium remain unknown. METHODS: The effects of propofol (1, 3, and 10 micrograms.ml-1) on the intrinsic contractility of left ventricular papillary muscles from normal hamsters and those with hypertrophic cardiomyopathy (strain BIO 14.6, aged 6 months) were investigated in vitro (Krebs-Henseleit solution, 29 degrees C, pH 7.40, Ca++ 2.5 mmol.l-1, stimulation frequency 3/min). RESULTS: Cardiac hypertrophy (143 +/- 13%, P < 0.001) was observed in cardiomyopathic hamsters. The contractility of papillary muscles from hamsters with cardiomyopathy was less than that of controls, as shown by the decrease in maximum shortening velocity (-29%, P < 0.03) and active isometric force (-51%, P < 0.001). Propofol did not induce any significant effect on contraction, relaxation, and contraction-relaxation coupling under low and high loads in normal hamsters. The effects of propofol were not significantly different between normal hamsters and those with cardiomyopathy. A slight but significant increase in maximum unloaded shortening velocity was observed in cardiomyopathic hamsters at 3 micrograms.ml-1 (4 +/- 6%, P < 0.05) and 10 micrograms.ml-1 (7 +/- 6%, P < 0.05). CONCLUSIONS: Propofol did not modify intrinsic myocardial contractility in normal hamsters, and no significant differences were observed between normal and cardiomyopathic hamsters. These results may be useful because, unlike propofol, most anesthetics decrease myocardial contractility. Nevertheless, indirect cardiac effects of propofol may be more important than its direct cardiac effects in patients with impaired cardiac function.

Animals↗

PubMed1995

In vitro effects of eltanolone on rat myocardium.

BACKGROUND: Eltanolone is a new short-acting intravenous induction agent. However, its effects on intrinsic myocardial contractility remain unknown. METHODS: The effects of eltanolone and its solvent (soya bean emulsion) on the intrinsic contractility of rat left ventricular papillary muscles were investigated in vitro (Krebs-Henseleit solution, 29 degrees C, pH 7.40, Ca2+ 0.5 mM, stimulation frequency 12 pulses/min). We studied contraction; relaxation; contraction-relaxation coupling under high and low loads; and postrest potentiation. RESULTS: Eltanolone (0.1, 0.3, 1, 3, and 10 micrograms.ml-1) induced no significant inotropic effect, as shown by the lack of changes in maximum unloaded shortening velocity and active isometric force. Eltanolone did not significantly modify the contraction-relaxation coupling under low load, suggesting that it did not modify calcium uptake by the sarcoplasmic reticulum. Eltanolone did not significantly modify the contraction-relaxation coupling under high load, suggesting that it did not modify calcium myofilament sensitivity. Eltanolone decreased the postrest potentiation in a concentration-dependent manner (from 150 +/- 14% to 118 +/- 9% at 10 micrograms.ml-1, P < 0.001), suggesting a decrease in the maximum capacity of calcium release by the sarcoplasmic reticulum, whereas its solvent did not. However, eltanolone did not slow postrest potentiation recovery, as shown by the absence of significant changes in the recovery slope, tau (4.5 +/- 1.4 vs. 3.8 +/- 1.0 beats; difference not statistically significant). CONCLUSIONS: Eltanolone induced no significant inotropic effect on rat myocardium. It induced a decrease in the calcium release function of the sarcoplasmic reticulum, but this effect was not sufficiently important to modify the inotropic properties.

Anesthetics, Intravenous↗

PubMed1995

Relations between myocardial contractility, myosin phenotype, and plasma angiotensin-converting enzyme activity in the cardiomyopathic hamster.

Angiotensin-converting enzyme (ACE) inhibitors have been shown to preserve myocardial contractility in the cardiomyopathic Syrian hamster (CSH). To determine if this was related to changes in myosin heavy-chain (MHC) phenotype, myosin isoform patterns and mechanical properties were studied in the same left ventricular papillary muscle from CSH of the Bio 53.58-dilated strain. From age 1 to 6 months, 22 CSH randomly received either perindopril 1 mg/kg/day in distilled water (PE, n = 11) or distilled water only (PL, n = 11), and seven control golden Syrian hamsters (C) received distilled water by force-feeding. Compared to C, PL had a lower Vmax (p < 0.01), a lower amount of alpha-MHC (p < 0.01), and an unchanged twitch duration. In PE, as compared to PL, there was a higher Vmax (p < 0.05), a higher alpha-MHC (p < 0.05), and an unchanged twitch duration. There was a positive relationship between Vmax and alpha-MHC in the population taken as a whole (p < 0.01), and when muscles from C and PL groups were plotted together (p < 0.001), but neither within each group, nor when PL and PE were plotted together. Our study indicates that in CSH (a) the preserved contractility with ACE-inhibitor treatment is associated with limitation of isomyosin shift induced by the myopathic process, but no cause-to-effect relationship could be demonstrated on the basis of our data, and (b) adaptive changes in twitch duration were not observed either in untreated CSH or in perindopril-treated CSH, despite significant changes in alpha-MHC content.

Animals↗

PubMed1995

M mode and Doppler echocardiographic assessment of left ventricular diastolic function in primary antiphospholipid syndrome.

BACKGROUND: High titres of serum antiphospholipid antibodies are a possible pathogenic factor for cardiac lesions in patients with systemic lupus erythematosus. OBJECTIVE: To test the hypothesis of a causal link between high titres of antiphospholipid antibodies in the serum and myocardial involvement in patients without systemic lupus erythematosus. PATIENTS AND DESIGN: 18 patients with primary antiphospholipid syndrome (recurrent fetal loss, arterial and/or venous thrombosis, high titres of antiphospholipid antibodies, and no criteria for systemic lupus erythematosus) were prospectively studied by cross sectional, M mode, and pulsed Doppler echocardiography, and compared with 18 healthy controls. The pulsed Doppler indices of left ventricular diastolic function included isovolumic relaxation time and four mitral outflow indices: peak velocity of early flow, peak velocity of late flow, early to late peak flow velocity ratio, and rate of deceleration of early flow. Four computerised M mode indices were also measured: peak rate of left ventricular enlargement in diastole, peak rate of posterior wall thinning, peak velocity of lengthening of the posterior wall, and velocity of circumferential chamber lengthening. RESULTS: Compared with controls, patients with primary antiphospholipid syndrome had higher values for isovolumic relaxation time and peak velocity of late mitral outflow and lower values for early to late mitral peak outflow velocity ratio, rate of deceleration of early mitral outflow, peak rate of left ventricular enlargement in diastole, peak rate of posterior wall thinning, peak velocity of lengthening of the posterior wall and velocity of circumferential chamber lengthening. CONCLUSION: This abnormal pattern reflects an impairment of myocardial relaxation and filling dynamics of the left ventricle in patients with primary antiphospholipid syndrome who were free of any clinically detectable heart disease. These data suggest that high serum titres of antiphospholipid antibodies may be associated with subclinical myocardial damage.

Adult↗

PubMed1995

Sarcoplasmic reticulum Ca2+ pumps in heart and diaphragm of cardiomyopathic hamster: effects of perindopril.

The polymyopathy of the Syrian hamster is associated with alterations of cellular calcium regulation and contractile performance of cardiac and skeletal muscles and, in particular, the diaphragm. Angiotensin-converting enzyme (ACE) inhibitors have been shown to preserve contractile performance. Therefore we analyzed the expression of the genes coding for the sarco(endo)plasmic reticulum Ca(2+)-adenosinetriphosphatase (SERCA) in heart and diaphragm of the cardiomyopathic Syrian hamster (CSH) from the dilated strain Bio 53-58, and we tested the influence of ACE inhibition on accumulation of the different SERCA mRNAs. In the diaphragm of healthy hamsters, two SERCA mRNA isoforms were present: SERCA 1 and SERCA 2. At 6 mo of age, the myopathic process resulted in decreased levels of SERCA 1, whereas the level of SERCA 2 was unchanged. The ACE inhibitor perindopril (1 mg.kg-1.day-1), administered by force feeding from 1 to 6 mo of age, had no effect on the SERCA 1 mRNA level. In heart, the myopathy was associated with a depressed level of SERCA 2 mRNA in 9- but not in 6-mo-old animals. Perindopril treatment from 6 to 9 mo reversed cardiac hypertrophy and the relative decrease in SERCA 2 mRNA level. Preventive treatment with perindopril from 1 to 9 mo tended to prevent (not significantly) the development of cardiac hypertrophy and reduction in SERCA gene expression. In conclusion, the myopathic process affects SERCA gene expression in the diaphragm and subsequently in the heart. Perindopril treatment can prevent SERCA mRNA loss in heart but not in diaphragm.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1995

Reactive hyperemia unmasks reduced compliance of cutaneous arteries in essential hypertension.

To evaluate changes in distal cutaneous arteries during hypertension, we used a noninvasive method to assess the compliance and vascular resistance of the hand radial arteries, mainly distributed to the skin, in 10 normotensive and 10 hypertensive (HT) men. Radial artery diameter and blood velocity were measured by means of pulsed Doppler concomitantly with measurements of finger arterial pressure by photoplethysmography. Hand radial vascular resistance was calculated as the ratio of mean arterial pressure to mean radial blood flow. A simple resistive-capacitive model of large and small arteries of the hand allowed us to evaluate arterial compliance from the exponential slope of finger diastolic pressure decay and vascular resistance. Measurements were made at baseline and during reactive hyperemia after 5 min of complete occlusion of the brachial artery with a pneumatic cuff. Except for pressure, there were no baseline differences between the groups. In normotensive and HT subjects, hyperemia increased radial artery diameter and blood velocity (P < 0.001) and compliance (P < 0.01 and P < 0.05, respectively) and decreased mean pressure (P < 0.01 and P < 0.001, respectively) and resistance (P < 0.001). During hyperemia, the only difference between the groups, except for pressure, was lower compliance in HT subjects (P < 0.01). Moreover, compliance during hyperemia negatively correlated with baseline mean pressure (P = 0.001). Thus hyperemia unmasked reduced compliance in the HT patients but did not show abnormal resistance, suggesting that the elastic properties of the hand skin radial arteries might be more sensitive than their resistive properties to high blood pressure.

Adult↗

PubMed1995

Effects of fatigue on force-velocity relation of diaphragm. Energetic implications.

Characteristics of the force (P)-velocity (V) relationship were investigated before and after fatigue in isolated diaphragm muscle of two species: mouse (n = 12), in which diaphragm is composed almost exclusively of fast-twitch fatigue-resistant fiber type, and rat (n = 12), in which diaphragm contains both fatigue-sensitive and fatigue-resistant fiber types. Following fatigue protocol, the mechanical performance of both the contraction and relaxation phases were significantly depressed in the two species. Consequences of the fatigue procedure on P-V characteristics differed markedly according to the two species. In mouse diaphragm, fatigue trial did not change the G curvature of the P-V hyperbola, the maximum mechanical efficiency Effmax, or the normalized peak power output M2. Conversely, in rat diaphragm, fatigue resulted in higher G curvature (p < 0.001), higher Effmax (p < 0.001) and a lower M2 (p < 0.001) compared with control values. This suggests that fatigue improved the economy of force generation in mixed rat diaphragm and not in mouse. This is consistent with an increased proportion of slow fatigue-resistant fibers caused by fatigue of fast fatigue-sensitive fibers in rat diaphragm.

Animals↗

PubMed1995

Contraction, relaxation, and economy of force generation in isolated human diaphragm muscle.

Contraction, relaxation, and energetics of normal human diaphragm strips (n = 10) were investigated over the whole load continuum in both twitch and tetanus modes. For a given level of isotonic total force and over a large part of the contraction phase, instantaneous velocity was shown to be a unique function of instantaneous length, regardless of time and initial length. In afterloaded tetanic contractions and over a wide range of loads, the peak lengthening velocity (VL) linearly decreased when maximum extent of muscle shortening (delta L) decreased. Stimulation mode modulated the VL versus delta L relationship, the slope of this linear regression being greater in tetanus than in twitch. Conversely, over a wide range of load, an increase in load linearly accelerated the peak rate of force decay, regardless of the stimulation mode. The energetics of human diaphragm muscle was evaluated in terms of both mechanical activity and economy of force generation. Maximum mechanical work (Wmax) differed significantly according to the stimulation mode, and the relative force at which Wmax occurred was higher in tetanus than in twitch (p < 0.05). The G curvature of the P-V hyperbola and maximum mechanical efficiency were significantly higher in tetanus than in twitch. This strongly suggests that the economy of force generation is higher in tetanus contractions than in twitch.

Adult↗