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Biomedical subjects

B Riou

Publications and source records attributed to B Riou.

At least 145 records · Page 8Linked to original sources
PubMed1991

Hemodynamic effects of hydroxocobalamin in conscious dogs.

Hydroxocobalamin has been shown to be a rapid and powerful antidote in acute cyanide poisoning and to prevent cyanide poisoning during sodium nitroprusside administration. However, its hemodynamic effects remain unknown. The authors therefore investigated the effects in chronically instrumented conscious dogs (n = 8) that were randomly given hydroxocobalamin (20, 70, and 140 mg.kg-1) or saline. Determination of peak cobalt plasma concentrations showed that 20 and 70 mg.kg-1 hydroxocobalamin correspond to "therapeutic doses," whereas 140 mg.kg-1 corresponds to a supratherapeutic dose. Hydroxocobalamin did not modify heart rate, mean arterial pressure, left ventricular (LV) end-diastolic pressure, and PR and QT intervals, regardless of the dose administered. The largest dose (140 mg.kg-1) induced a decrease in the maximum increase of LV pressure (-7 +/- 3%; P less than 0.05), maximum aortic blood flow acceleration (-17 +/- 5%; P less than 0.05), and cardiac output (-19 +/- 6%; P less than 0.05), whereas systemic resistance increased (+41 +/- 9%; P less than 0.05). In six other dogs, local administration of hydroxocobalamin (0.5, 1.5, and 5.0 mg.kg-1.min-1) confirmed that, in large doses, this drug has direct vasoconstrictor properties affecting both conductance (decrease in iliac artery diameter: -2.5 +/- 0.8%) and resistance (decrease in iliac artery blood flow: -19.5 +/- 3.4%) vessels. Thus, hydroxocobalamin should be a safe cyanide antidote, considering the lack of hemodynamic effects within the therapeutic range of doses.

Animals↗
PubMed1991

Ventilatory effects of medical antishock trousers in healthy volunteers.

The ventilatory effects of medical antishock trousers (MAST) were investigated using 10 healthy volunteers. Use of the MAST (60-80 mm Hg) decreased forced expiratory volume (-8% +/- 4%, p less than 0.01), vital capacity (-8% +/- 5%, p less than 0.01), and functional residual capacity (-12% +/- 6%, p less than 0.01) and induced a significant decrease in tidal volume (-30% +/- 17%, p less than 0.05), but minute ventilation was unmodified because of a concomitant increase in respiratory rate (+17% +/- 8%, p less than 0.001). The MAST modified the breathing pattern: the abdominal contribution to ventilation was markedly decreased (-57% +/- 22%, p less than 0.001), suggesting a decrease in the diaphragmatic contribution to ventilation. The MAST increased both the end-expiratory (+131% +/- 115%, p less than 0.01) and inspiratory variation (delta Pgas: +42% +/- 40%, p less than 0.05) of gastric pressure, whereas the end-expiratory and inspiratory variation of esophageal pressure remained unchanged. Because of a higher delta Pgas, the dynamic compliance of the abdominal compartment markedly fell (-77% +/- 10%, p less than 0.001). Transdiaphragmatic pressure (Pdi: +28% +/- 30%, p less than 0.05) significantly increased and the pressure-time index of the diaphragm significantly increased (+32% +/- 32%, p less than 0.05) after inflation of the MAST, suggesting an increase in the diaphragmatic cost of breathing. Inspiratory activity of the parasternal intercostal muscles significantly increased after the MAST was inflated. Computerized tomography showed that the MAST induced a cephalad shift of the diaphragm, which reduced pulmonary height.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Hypertonic sodium chloride and hemorrhagic shock].

Numerous experimental studies on the effects of hypertonic saline in haemorrhagic shock have been published and controlled clinical studies are now beginning to be reported. Animals suffering from an otherwise lethal haemorrhagic shock survived when given hypertonic sodium chloride solution (7.5%, 2,400 mosmol.1-1). In most studies, this solution was more efficient than isotonic fluids in treating controlled haemorrhage. Although the mechanisms involved are not yet fully understood, they certainly include the following: 1) plasma volume expansion due to osmotic fluid shifts into the vascular compartment from intra- and extra-cellular fluid reservoirs, as hypertonic saline induces hypernatraemia and hyperosmolarity, both effects linked to the sodium load; 2) non specific precapillary vasodilation of renal, coronary and splanchnic vessels; 3) arterial and venous vasoconstriction in muscle and skin, due to a vagal reflex set off by the lung osmoreceptors, the efferent pathway of which is likely to be the sympathetic nervous system; 4) increased myocardial contractility. Hypertonic saline also decreases intracranial pressure, and improves lung function during resuscitation of haemorrhagic shock. However, hypertonic saline should not yet be used routinely in man, except in controlled clinical studies. Indeed, there are as yet not enough data concerning humans. Moreover, during uncontrolled haemorrhage, hypertonic saline increased blood pressure, and therefore bleeding, thus reducing survival rates. Further clinical studies are required before hypertonic saline could be safely recommended for treatment of haemorrhagic shock.

Animals↗
PubMed1990

[Respiratory tract obstruction caused by ballooning of an intubation tube cuff during nitrous oxide inhalation].

A typical case of upper airway obstruction due to deformation of a low pressure tracheal tube cuff is reported. It would seem that this herniation may have been due to nitrous oxide diffusing with in the air-filled cuff, thereby causing it to overdistend. This increase in pressure occurred after 3 hours of inhalation of a mixture of oxygen and nitrous oxide. The deformed cuff may either block the lumen at the end of the tube, or push the tube against the tracheal wall. The result is, in either case, a mechanical obstruction of the airway, with hypoxia, and then anoxia. In the reported case, it was the decrease of SpO2 which alerted the anaesthetist. Pulse oximetry was helpful for an early diagnosis. To avoid such accidents, it is suggested either to inflate the cuff with the gas mixture with which the patient is ventilated, or to deflate it every 30 min.

Adult↗
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↗
PubMed1990

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

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

Animals↗
PubMed1989

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

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

Animals↗
PubMed1989

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

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

Adrenergic alpha-Agonists↗
PubMed1989

Inotropic effect of ketamine on rat cardiac papillary muscle.

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

Animals↗