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Biomedical subjects

D Chemla

Publications and source records attributed to D Chemla.

88 records · Page 5Linked to original sources
PubMed1990

Effect of beta adrenoceptors and thyroid hormones on velocity and acceleration of peripheral arterial flow in hyperthyroidism.

Brachial artery flow patterns were studied in 10 hyperthyroid and 10 normal subjects. Mean blood velocity and flow were evaluated by pulsed Doppler, and peak systolic acceleration was calculated by computer-assisted digitization of the instantaneous velocity curve. Compared to control subjects, hyperthyroid patients had higher velocity and flow (p less than 0.01, p less than 0.02) and higher peak systolic acceleration (p less than 0.01). In hyperthyroid patients, measurements were repeated after (1) mechanical exclusion of the hand from brachial circulation, (2) short-term beta-blocker treatment and (3) inducement of the euthyroid state. Exclusion of the hand reduced velocity and flow (p less than 0.001) but did not change peak systolic acceleration. Beta blockade induced disparate changes of velocity and flow but reduced peak systolic acceleration (p less than 0.05). In the euthyroid state, decreased blood velocity (p less than 0.01), flow (p less than 0.02) and acceleration (p less than 0.02) were observed. A hyperkinetic arterial circulation consisting of an increase in both velocity and acceleration is thus observable in hyperthyroidism. Hand exclusion showed that velocity seems to be influenced by peripheral factors while beta blockade suggests that acceleration is dependent of beta 1 adrenoceptors. Comparison between euthyroidism and hyperthyroidism indicates that both mean blood velocity and peak systolic acceleration are influenced by thyroid hormones.

Adrenergic beta-Antagonists↗
PubMed1990

Beta blockers induce different intrarenal effects in humans: demonstration by selective infusion of tertatolol and propranolol.

The effects of tertatolol and propranolol on renal circulation were studied in patients with normal renal function to test the hypothesis that various beta blockers may have different vasomotor effects within the renal vascular bed. Left renal blood flow was measured by the continuous thermodilution method before (t0), and 5 (t1), 10 (t2), 20 (t3), and 30 (t4) minutes after a selective infusion of tertatolol (0.25 mg, N = 4) or propranolol (2.5 mg, N = 4) into the left renal artery. Heart rate, cardiac output, aortic and right atrial pressures, and systemic vascular resistances did not significantly vary after either drug throughout the study. Plasma renin activity and plasma aldosterone in arterial and renal venous blood started to decrease at t1 after each drug. After propranolol, renal blood flow, renal vascular resistance and the renal arteriovenous oxygen difference were unchanged. Conversely, after tertatolol at t3, renal blood flow was increased (from 426 +/- 18 mL/min/1.73 m2 to 509 +/- 56 mL/min/1.73 m2, P = .03), renal vascular resistance and renal arteriovenous oxygen difference were decreased (P less than .001), and the renal blood flow/cardiac output ratio was increased (P = .03). The filtration fraction did not vary after either drug, as attested by the unchanged polyfructosan extraction coefficient. This clinical study shows that selective infusion of a single low dose of tertatolol into the renal artery results in a delayed intrarenal vasodilator effect, while at the dose tested propranolol does not modify renal hemodynamics.

Adrenergic beta-Antagonists↗
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

[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↗
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

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↗
PubMed1984

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↗
PubMed1983

[Bird fancier's lung and Crohn disease. Apropos of a case].

The case of pigeon breeders' disease reported here is peculiar not only because of the large number of birds with which the patient was in contact, but also because the disease developed in a patient presenting with both pulmonary tuberculosis and Crohn's disease. Moreover, 18 months after eviction of the birds and beginning of corticosteroid therapy, the number of lymphocytes in fluid from broncho-alveolar lavage remained high.

Alveolitis, Extrinsic Allergic↗