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Biomedical subjects

Y Lecarpentier

Publications and source records attributed to Y Lecarpentier.

At least 109 records · Page 6Linked to original sources
PubMed1993

[Protective effects of perindopril in an experimental model of cardiomyopathy].

The effects of an angiotensin converting enzyme (ACE) inhibitor on the intrinsic contractility of the myocardium in cardiac failure have not been studied intensively. The authors studied inotropism, lusitropism and economy of contraction in vitro on left ventricular papillary muscle preparations of cardiomyopathic Syrian hamsters (CSH) treated preventively with perindropil, i.e. before overt signs of cardiac failure. The CSH of the dilated Bio 53.58 strain aged 1 month were treated with perindropil 1 mg/Kg/day for 5 months (PE, N = 11) or with placebo (PL, N = 11) and control hamsters of the F1B strain received placebo (C, N = 7). Compared with C, PL had a significant reduction of the maximal velocity of contraction Vmax (p < 0.01) and of total isometric tension (TF/mm2), p < 0.05, and a reduction of the G curve of the hyperbolic Hill Force-Velocity relationship (p < 0.01). The G value is usually greater in models with improved economy of contraction. When compared with PL, PE showed a 68% inhibition of the plasma activity of ACE, a better Vmax (p < 0.05) but an unchanged TF/mm2. The G value was less depressed than that of C (p < 0.05). The velocity of isotonic relaxation (maxVL) and the negative peak of the derivative of the isometric force (-dF/dt max) were significantly lower in the PL than in the C group but these lusitropic abnormalities remained coordinated with those of the contraction phase, indicating the absence of an intrinsic effect on relaxation in cardiomyopathy. Perindopril prevented the reduction of maxVL but not that of -dF/dt max.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

Myocardial contractility, lusitropy and calcium responsiveness in young (50 days) and hypertrophied (180 days) cardiomyopathic hamsters.

Contractility, lusitropy and responsiveness to the increase of external Ca2+ concentration were studied in left ventricular papillary muscles of normal and cardiomyopathic Syrian hamsters (SCH) from the UM-X 7.1 strain, both at the onset of myolysis (50-day-old animals) and at the cardiac hypertrophy stage (180-day-old animals) in the absence of congestive heart failure. A marked decrease in all indices of systolic performance was observed in 180-day-old myopathic hamsters as compared to age-matched controls. This was associated with (1) an impairment of the relaxation phase, (2) a loss of the load sensitivity of relaxation, and (3) a decrease in the inotropic and lusitropic responsiveness to Ca2+. On the other hand, when some indices of contraction and the inotropic response to Ca2+ were impaired in 50-day-old myopathic hamsters as compared to age-matched controls, relaxation phase and the lusitropic response to Ca2+ did not alter. This study shows that, in the UM-X 7.1 myopathic hamsters at the earlier stage of the disease, alterations in calcium homeostasis and contraction seem to be the first determinant factors of the development of heart failure when relaxation is not impaired. Conversely, when cardiac hypertrophy has developed, impaired relaxation may worsen heart failure.

Age Factors↗
PubMed1992

Spontaneous arrhythmias in various models of cardiac hypertrophy and senescence of rats. A Holter monitoring study.

OBJECTIVE: The aim was to define experimental models of spontaneous arrhythmias in various models of cardiac hypertrophy in rats. METHODS: Cardiac hypertrophy was induced by several methods and 24 h Holter monitoring was recorded in conscious rats to quantify spontaneous arrhythmias in hypertrophied hearts. Male Wistar rats were studied. A group of young controls 1-2 months old (n = 16) was compared to four groups of animals with cardiac hypertrophy: (1) thyrotoxic rats which received a daily intraperitoneal injection of L-thyroxine for 7 d (n = 6); (2) rats subjected to abdominal suprarenal aortic stenosis (n = 11); (3) senescent rats 22-24 month old (n = 6); and (4) S-DOCA-salt (senescent animals rendered hypertensive by uninephrectomy and DOCA-salt treatment, n = 8). RESULTS: (1) Thyroxine resulted in 20% cardiac hypertrophy, with normal arterial tension, sinus tachycardia, a shorter P wave length and PR interval, and frequent (5/6) atrioventricular block. No premature beats were seen. (2) In aortic stenosis, atria and left ventricle were hypertrophied by 53% and systolic carotid pressure increased by 63%. The incidence of supraventricular premature beats was increased [frequency = 0.70 (SEM 0.3) per 24 h in control v 99(61) in aortic stenosis, p < 0.05]. Ventricular premature beats remained as rare as in control. (3) In senescent and S-DOCA-salt rats all types of spontaneous arrhythmias, but specially supraventricular arrhythmias and atrioventricular block, were frequent. Cardiac hypertrophy produced by DOCA-salt treatment in senescent rats had no effect on the incidence and nature of arrhythmias, but resulted in an increased QTc interval. CONCLUSIONS: Senescent rats and rats with aortic stenosis represent valid models of spontaneous arrhythmias occurring in the absence of ischaemia or toxic insult. Spontaneous arrhythmias in rats are mainly of supraventricular origin. Hyperthyroidism in rats is a model of atrioventricular block probably related to tachycardia. Holter monitoring in rats may have several potential pathophysiological and pharmacological applications.

Aging↗
PubMed1992

In vitro effects of propofol on rat myocardium.

Propofol is a short-acting intravenous induction agent that induces cardiovascular depression. However, the effects of propofol on intrinsic myocardial contractility remain debatable. Thus, we studied the effects of three concentrations of propofol (1, 3, and 10 micrograms.ml-1, respectively) and its solvent on the mechanics and energetics of isolated rat left ventricular papillary muscles. Propofol and its solvent did not induce any significant inotropic effect as shown by the lack of significant changes in maximum unloaded shortening velocity and in active isometric force. Nevertheless, propofol induced a slight decrease in isometric force (92 +/- 6%, 95 +/- 5%, and 95 +/- 4%, respectively, all P less than 0.01) under certain experimental conditions (i.e., after isometric stabilization). Using various afterloaded twitches, the peak power output and the curvature of the force-velocity curve were calculated. Propofol and its solvent did not significantly modify these two energetic parameters, indicating that it did not change myothermal economy and cross-bridge kinetics. Propofol impaired isotonic relaxation, suggesting that it decreased calcium uptake by the sarcoplasmic reticulum, whereas its solvent alone did not. However, alteration of sarcoplasmic reticulum function was moderate, since postrest potentiation and postrest recovery were unmodified after propofol. It was concluded that propofol induces moderate changes on intrinsic myocardial contractility. These results suggest that cardiovascular depression observed with propofol in vivo is not related to intrinsic myocardial depression.

Animals↗
PubMed1992

[Effects of angiotensin II on intrinsic contractibility of the myocardium in the guinea pig].

Analysis of the contraction-relaxation coupling of guinea pig left ventricular papillary muscle was performed with and without angiotensin II (Ang II 10-6 M). The inotropic and lusitropic properties of Ang II were evaluated at 20 degrees C, 30 beats/min, CaCl2 6H20 2 mM and pH 7.4, under low load (isotonic conditions) and high load (isometric conditions). The maximum velocity of contraction (max Vc) and relaxation (max Vr) were calculated from isotonic contraction having as its only load that corresponding to the imposed preload at Lmax. The maximum positive (+dF/dtmax) and negative values (-dF/dtmax) of the derivative of the force were calculated during isometric contraction. The coefficients, R1 = max Vc/max Vr and R2 = (+dF/dtmax)/(-dF/dtmax), were calculated. These two coefficients allow the contraction-relaxing coupling to be assessed at low and high loads respectively. In the presence of Ang II, the increase in the isotonic velocity of relaxation (1.93 +/- 0.26 vs 3.15 +/- 0.35 Lmax/sec; p < 0.001) was greater than that of the isotonic velocity of contraction (0.74 +/- 0.05 vs 1.02 +/- 0.07 Lmax/sec; p < 0.001). This results in a decrease in the ratio of the velocities of isotonic contraction and relaxation (R1) (0.44 +/- 0.06 vs 0.35 +/- 0.05; p < 0.01). Under isometric conditions, Ang II induced a proportional increase in the parameters of contraction and relaxation. Consequently, there was no significant change in the R2 coefficient (1.22 +/- 0.06 vs 1.12 +/- 0.08). Moreover, Ang II did not induce any change in the sensitivity of the relaxation with respect to load.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1992

Positive inotropic effects of RP 62719, a new pure class III antiarrhythmic agent, on guinea pig myocardium.

The mechanical effects of RP 62719 [(-)1-[-2-(3,4-dihydro-2H-1- benzopyran-4-yl)ethyl]-4-(3,4-dimethoxyphenyl)-piperidine] were tested in vitro on guinea pig left ventricular papillary muscle. RP 62719 is a novel pure class III antiarrhythmic agent known to prolong the cardiac action potential duration by selectively blocking the inward rectifying K+ current. Mechanical parameters were determined from contraction and relaxation phases under isotonic and isometric conditions. At a concentration of 0.02 microM, RP 62719 did not produce significant effects on inotropy or lusitropy. At 0.2 and 2 microM, the drug improved contraction under both heavy and low loading conditions, as evidenced by a 30% increase in maximum unloaded shortening velocity (Vmax, P < .001), peak amplitude of shortening (delta L, P < .001), peak isometric active force normalized per cross-sectional area (AF/s, P < .001) and positive peak of the force derivative per mm2 (+dF/s, P < .001). At the same concentrations, positive lusitropic effects were evidenced by an increase in maximum lengthening velocity (maxVr) and negative peak of force derivative per mm2 (-dF/s, P < .001). At a higher concentration (20 microM), effects of RP 62719 on inotropy and lusitropy were less marked, thus accounting for the bell-shaped form of the dose-response curve. An increase in the extracellular Ca++ concentration from 2.5 to 3.75 mM improved inotropy to a similar extent (+30-50%) as did 2 microM RP 62719. However, lusitropy and mechanical coupling between contraction and relaxation were not modified in the same proportion under RP 62719 and under 3.75 mM Ca++.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Effects of perindopril on myocardial inotropy, lusitropy and economy, and on diaphragmatic contractility in the cardiomyopathic Syrian hamster.

Over a 5-month period, 22 1-month-old cardiomyopathic Syrian hamsters were randomly treated with either angiotensin-converting enzyme inhibitor (perindopril 1 mg/kg/day) (PE, n = 11) or placebo (PL, n = 11), and 7 age-matched controls (C) were given placebo. Compared to C, mechanics of left ventricular papillary muscles from PL exhibited a lower maximum unloaded shortening velocity (Vmax) (P less than .01) and normalized peak active force (P less than .05), and a significantly less curved shape of the force-velocity (F-V) relationship (P less than .01). The curvature of the F-V relationship has been proposed as a reflection of the efficiency of muscle contraction. Compared to PL, PE had a 68% inhibition of plasma ACE activity and a greater Vmax (P less than .05), whereas active force (AF) was similar. This resulted in a lesser decrease of the curvature of the F-V relationship compared to that of C (P less than .05). Muscle strips from the ventral costal diaphragm were dissected from the muscle in situ. In both twitch and tetanus modes, intrinsic mechanical performance of diaphragm muscle was markedly decreased in PL compared to C as regards normalized positive (+dF/dtmax/mm2) and negative (-dF/dtmax/mm2) peak rate of force, and normalized peak active force (AF/mm2) (P less than .01 each). In both twitch and tetanus modes, PE had an increased +dF/dtmax/mm2 (P less than .05), -dF/dtmax/mm2 and AF/mm2 (P less than .01 each), compared to PL. These results indicate 1) that the low inotropic state observed in cardiomyopathic Syrian hamsters was associated with decreased myothermal economy of cardiac contraction and with a major impairment of diaphragm intrinsic contractility, and 2) that early therapy with angiotensin-converting enzyme inhibitor helped to preserve myocardial contractility and economy, and diaphragm contractility.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

Elevated blood cyanide concentrations in victims of smoke inhalation.

BACKGROUND: The nature of the toxic gases that cause death from smoke inhalation is not known. In addition to carbon monoxide, hydrogen cyanide may be responsible, but its role is uncertain, because blood cyanide concentrations are often measured only long after exposure. METHODS: We measured cyanide concentrations in blood samples obtained at the scene of residential fires from 109 fire victims before they received any treatment. We compared the results with those in 114 persons with drug intoxication (40 subjects), carbon monoxide intoxication (29 subjects), or trauma (45 subjects). The metabolic effect of smoke inhalation was assessed by measuring plasma lactate at the time of admission to the hospital in 39 patients who did not have severe burns. RESULTS: The mean (+/-SD) blood cyanide concentrations in the 66 surviving fire victims (21.6 +/- 36.4 mumol per liter, P less than 0.001) and the 43 victims who died (116.4 +/- 89.6 mumol per liter, P less than 0.001) were significantly higher than those in the 114 control subjects (5.0 +/- 5.5 mumol per liter). Among the 43 victims who died, the blood cyanide concentrations were above 40 mumol per liter in 32 (74 percent), and above 100 mumol per liter in 20 of these (46 percent). There was a significant correlation between blood cyanide and carbon monoxide concentrations in the fire victims (P less than 0.001). Plasma lactate concentrations at the time of hospital admission correlated more closely with blood cyanide concentrations than with blood carbon monoxide concentrations. Plasma lactate concentrations above 10 mmol per liter were a sensitive indicator of cyanide intoxication, as defined by the presence of a blood cyanide concentration above 40 mumol per liter. CONCLUSIONS: Residential fires may cause cyanide poisoning. At the time of a patient's hospital admission, an elevated plasma lactate concentration is a useful indicator of cyanide toxicity in fire victims who do not have severe burns.

Adolescent↗
PubMed1991

Effects of hydroxocobalamin on rat cardiac papillary muscle.

Hydroxocobalamin is a rapid and powerful antidote in acute cyanide poisoning. The effects of hydroxocobalamin (0.1, 0.3, and 1 mM) on intrinsic myocardial contractility were studied on isolated rat cardiac papillary muscles (n = 10). Whatever the concentration, hydroxocobalamin did not modify the active isometric force and a slight increase in maximum unloaded shortening velocity was noted at 1 mM. Only 0.3 mM significantly impaired contraction-relaxation coupling under low load, suggesting a slight decrease in sarcoplasmic reticulum function. No changes in contraction-relaxation coupling under heavy load were noted, suggesting the lack of modification of myofilament calcium sensitivity. These results suggest that hydroxocobalamin does not induce noticeable changes in intrinsic myocardial contractility. An indirect mechanism might be involved in the previously reported decrease in cardiac function at supratherapeutic concentrations of hydroxocobalamin.

Animals↗
PubMed1991

[Cardiomyopathy in the Syrian hamster. Physiological and therapeutic aspects].

The primary hereditary cardiomyopathy of the Syrian hamster is a particularly interesting model of experimental cardiomyopathy 1) because of its slow progression to cardiac failure unlike acute experimental volume and pressure overloading; 2) because of the reproducibility and predictable nature of the mechanical, biochemical and electrophysiological abnormalities observed at each stage of the disease; 3) because of involvement of other muscle groups, and particularly, skeletal muscle. The physiopathology is not fully understood but a disturbance of intracellular calcium homeostasis appears to play a major role. From the therapeutic point of view, a number of calcium antagonists have been shown to be effective in restoring myocardial function, but they have no effect on skeletal muscular lesions. Recently, early prophylactic intervention with therapeutic doses of perindopril has been shown to prevent the decrease of certain parameters of myocardial contractility in vitro in the dilated group, before the appearance of any signs of cardiac failure. This study also showed that angiotensin converting enzyme inhibitors had no intrinsic negative inotropic effects.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

The contraction-relaxation coupling during pressure-induced cardiac hypertrophy.

Contraction-relaxation coupling was studied in rat and guinea-pig papillary muscles during chronic pressure overload induced by aortic stenosis and during acute hypoxia. Coefficient R1 (ratio between maximum shortening and lengthening velocities of the isotonic twitch loaded with preload only) and coefficient R2 (ratio between the positive and negative peak force derivatives of the isomeric twitch) tested the contraction-relaxation coupling under low and heavy load respectively. Cardiac hypertrophy was similar in guinea-pigs (+43 +/- 5%) and rats (+55 +/- 7%). In both species, cardiac hypertrophy significantly impaired contraction and relaxation phases. In the rat, neither R1 (-1 +/- 4%) nor R2 (-5 +/- 4%) varied significantly during cardiac hypertrophy whereas, in the guinea-pig, an increase in R1 (+56 +/- 18%), P less than 0.001) and in R2 (+26 +/- 9%, P less than 0.01) was noted. These species-related differences might be linked in part to differences in sarcoplasmic reticulum function and myosin ATPase activity. Acute hypoxia, which leads to a decrease in cellular ATP levels, was responsible for a marked decrease in myocardial performance, while R1 increased (+66 +/- 8%, P less than 0.05) and R2 decreased (-14 +/- 1%, P less than 0.05). These results showed that chronic pressure overload modified the contraction-relaxation coupling in a characteristic manner according to the species studied and these changes differed from those observed during acute hypoxia.

Animals↗
PubMed1990

In vitro effects of etomidate on intrinsic myocardial contractility in the rat.

Etomidate is available in two different solvents: propylene glycol for induction of anesthesia and ethanol for maintenance of anesthesia. The direct effect of etomidate (1 and 5 micrograms/ml) and of its solvents on cardiac muscle was studied using rat left ventricular papillary muscle. Etomidate induced a slight positive inotropic effect in both solvents, as shown by an increase in maximum unloaded shortening velocity (Vmax) but not in force. At 0.5 mM Ca++ 5 micrograms/ml etomidate increased Vmax (128 +/- 18%, P less than 0.05) but not force (103 +/- 16%, NS). Using various afterloaded twitches, the peak power output (Emax) was calculated: 1 and 5 micrograms/ml etomidate increased Emax (107 +/- 8%, P less than 0.05, and 108 +/- 10%, P less than 0.05, respectively). This increase was related to the increase in Vmax and not in isometric force. Etomidate did not modify the elastic components of papillary muscle, isometric relaxation, and contraction-relaxation coupling under high load. Several findings suggest that etomidate in propylene glycol impaired the sarcoplasmic reticulum (SR) function: 1) it impaired the isotonic relaxation, the contraction-relaxation coupling under low load, and the load sensitivity of relaxation; and 2) it decreased postrest potentiated contraction, which is highly dependent on the SR. Nevertheless, alteration of SR function was only significant at high [Ca++]o and the beat-to-beat postrest recovery was not modified, indicating that the deleterious effects on SR function were moderate. The isotonic relaxation (max Vr) was more impaired by etomidate in propylene glycol (78 +/- 9%, P less than 0.001) and by propylene glycol alone (69 +/- 9%, P less than 0.001) than by etomidate in ethanol (97 +/- 12%, NS) and by ethanol alone (92 +/- 8%, P less than 0.05). This suggests that propylene glycol was responsible for the decrease in SR function. Etomidate in propylene glycol thus has a dual action on rat myocardium: 1) a slight positive inotropic effect due to etomidate per se, and 2) a slight decrease in SR function probably related to propylene glycol. However, because etomidate in propylene glycol induced a slight decrease in isometric force under certain experimental conditions (i.e., after isometric stabilization), etomidate in propylene glycol may induce a slight negative inotropic effect in some clinical conditions as a result of its dual action on the myocardium.

Animals↗
PubMed1990

Effects of ketamine on the cardiac papillary muscle of normal hamsters and those with cardiomyopathy.

The effect of ketamine (10(-5) and 10(-4) M) on the intrinsic contractility of left ventricular papillary muscle from normal hamsters and those with cardiomyopathy (BIO 82.62, 6-month old) was investigated. At these concentrations, ketamine induced a positive inotropic effect on normal papillary muscle, as shown by an increase in maximum unloaded shortening velocity (+19 +/- 4 and +34 +/- 5%, P less than 0.05), active isometric force (+32 +/- 8 and +57 +/- 11%, P less than 0.05), and peak power output (+40 +/- 8 and +80 +/- 16%, P less than 0.05), and induced a slight decrease in sarcoplasmic reticulum function. Ketamine had no effect on the curvature of the total force-velocity curve, suggesting that it does not modify myothermal economy. Contractility of papillary muscle from hamsters with cardiomyopathy was less than that of controls, as shown by the decrease in isometric active force (-41%, P less than 0.02), peak power output (-33%, P less than 0.05), and sarcoplasmic reticulum function. The positive inotropic effect of ketamine on papillary muscle from hamsters with cardiomyopathy was less marked than in controls and almost suppressed in some cases: only the maximum unloaded shortening velocity was significantly increased with 10(-5) M ketamine (+7 +/- 6%, P less than 0.05), whereas no significant changes were observed in active isometric force (+14 +/- 8 and +13 +/- 11%; nonsignificant [NS]) and peak power output (+9 +/- 5 and +13 +/- 8%; NS) with ketamine (10(-5) and 10(-4) M, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

In vitro demonstration of the antidotal efficacy of hydroxocobalamin in cyanide poisoning.

The effects of sodium cyanide (1 mM) and the antidotal action of hydroxocobalamin (1 mM) were studied on rat cardiac papillary muscle. A 10-min period of exposure to cyanide induced a marked decrease in inotropy as shown by a decrease in the maximum unloaded shortening velocity (Vmax: 64 +/- 11% of precyanide values, p <0.01) and active isometric force (AF/s: 35 +/- 13%, p <0.01). The impairment of contraction-relaxation coupling under low load and the nearly complete disappearance of the load sensitivity of relaxation suggested a decrease in sarcoplasmic reticulum function. The proportional acceleration in isometric relaxation suggested a decrease in myofilament calcium sensitivity. There was a nearly complete recovery from cyanide poisoning after 5 min of exposure to hydroxocobalamin, whereas in a control group receiving cyanide alone, the mechanical parameters remained unchanged or were further impaired. The effects of hydroxocobalamin developed very quickly, beat to beat. The main toxic target of cyanide is brain and heart cytochrome oxidase, and brain damage appears only a few minutes after the onset of anoxia. Because hydroxocobalamin is a rapid and powerful antidote, it may be useful in the treatment of acute cyanide poisoning.

Journal Article↗
PubMed1990

Effects of chronic growth hormone hypersecretion on intrinsic contractility, energetics, isomyosin pattern, and myosin adenosine triphosphatase activity of rat left ventricle.

We studied papillary muscle mechanics and energetics, myosin phenotype, and ATPase activities in left ventricles from rats bearing a growth hormone (GH)--secreting tumor. 18 wk after tumor induction, animals exhibited a dramatic increase in body weight (+101% vs. controls) but no change in the ventricular weight/body weight ratio. The maximum isometric force of papillary muscles normalized per cross-sectional area rose markedly (+42%, P less than 0.05 vs. controls), whereas the maximum unloaded shortening velocity did not change. This was observed despite a marked isomyosin shift towards V3 (32 +/- 5% vs. 8 +/- 2% in controls, P less than 0.001). Increased curvature of the force-velocity relationship (+64%, P less than 0.05 vs. controls) indicated that the muscles contracted more economically, suggesting the involvement of V3 myosin. Total calcium- and actin-activated myosin ATPase activities assayed on quickly frozen left ventricular sections were similar in tumor-bearing rats and in controls. After alkaline preincubation, these activities only decreased in tumor-bearing rats, demonstrating that V3 enzymatic sites were involved in total ATPase activity. These data demonstrate that chronic GH hypersecretion in the rat leads to a unique pattern of myocardial adaptation which allows the muscle to improve its contractile performance and economy simultaneously, thanks to myosin phenoconversion and an increase in the number of active enzymatic sites.

Actomyosin↗
PubMed1990

[Effects of alpha adrenergic stimulation on the mechanical properties of the myocardium].

The mechanical effects of phenylephrine at 2 x 10(-6) M (PE1, n = 8), 2 x 10(-5) M (PE2, n = 10) and 2 x 10(-4) M (PE3, n = 6) were studied on rat left ventricular papillary muscle, in the presence of propranolol (4 x 10(-7) M) and 0.5 mM of (Ca2+)e. The contraction-relaxation coupling was studied under isotonic and isometric conditions. The maximal velocity of contraction (max Vc) and relaxation (max Vr) were calculated during isotonic contraction with preload only at L max. The positive (+ dF/dt max) and negative (- dF/dt max) peaks of the derivative of the force were calculated during isometric contraction. Two coefficients, R1 = max Vc/max Vr and R2 (+ dF/dt max)/(- dF/dt max) provided an appreciation of the contraction-relaxation coupling at low and high loads respectively. The positive inotropic effect observed in the three groups was accompanied by a significant decrease of the coefficient R1 (PE1: - 11 +/- 2% p less than 0.001; PE2: - 15 +/- 2%, p less than 0.001; PE3: -20 +/- 2%, p less than 0.001). On the other hand, no significant variations of the coefficient R2 were observed (PE1: 3 +/- 3%; PE2: 1 +/- 4%; PE3: 5 +/- 3%). The proportionally greater improvement in the velocity of relaxation compared to the velocity of contraction at low loads suggests that the sarcoplasmic reticulum is involved in the expression of positive inotropic and positive lusitropic effects of alpha-adrenergic stimulation.

Adrenergic alpha-Agonists↗
PubMed1990

[Changes in contraction-relaxation coupling in experimental cardiac hypertrophy in the guinea pig].

Guinea pig myocardium resembles human myocardium with respect to the mechanisms which regulate contractility (enzymatic activity of myosine, functional activity of the sarcoplasmic reticulum). Guinea pig left ventricular hypertrophy (LVH) is therefore a good experimental model for the study of human LVH. The mechanical properties of 5 months old female guinea pigs' left ventricular papillary muscle, 3 weeks after constriction of the abdominal aorta (N = 10), were investigated. Ten papillary muscles of operated control animals and eight of normal guinea pigs submitted to 20 minutes hypoxia were also studied. The animals had no signs of cardiac failure after constriction of the abdominal aorta but the increase in the ratio of heart to body weight (p less than 0.001) confirmed the LVH. When compared with the operated controls, there was a decrease of the maximum velocity of contraction at zero load, of the velocity of contraction with preload alone (Vc), of the total isometric force normalized for the section of the muscle(s) and of the positive peak of the derivative of the isometric force normalized for section (+ dF/s) (p less than 0.001 for each parameter). The parameters of relaxation were also abnormal: decreased velocity of isotonic relaxation with preload only (Vr) and of the negative peak of the derivative of the isometric force normalized for section (- dF/s) (p less than 0.001 for each parameter), and an increase in the half relaxation time (t1/2) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗