Treatment of the biodegradable fraction of used disposable diapers by co-digestion with waste activated sludge.

The results presented in this paper are part of a project aimed at designing an original solution for the treatment of used disposable diapers permitting the recycling of materials and the recovery of energy. Diapers must be collected separately at source and transported to an industrial facility to undergo special treatment which makes it possible to separate plastics and to recover a biodegradable fraction (BFD) made up mainly of cellulose. The methane yield of BFD was measured and found to be 280 ml CH4/g VSfed on average. 150 kg of dry BFD can be retrieved from the treatment of one ton of used disposable diapers, representing an energy potential of about 400 kW h of total energy or 130 kW h of electricity. As the treatment process for used diapers requires very high volumes of water, the setting up of the diaper treatment facility at a wastewater treatment plant already equipped with an anaerobic digester offers the advantages of optimizing water use as well as its further treatment and, also, the anaerobic digestion of BFD. The lab-scale experiments in a SBR showed that BFD co-digestion with sewage sludge (38% BFD and 62% waste activated sludge on volatile solids basis) was feasible. However, special attention should be paid to problems that might arise from the addition of BFD to a digester treating WAS such as insufficient mixing or floating particles leading to the accumulation of untreated solids in the digester.

[Magnetocardiography: principles and potential uses in cardiology]. / La magnétocardiographie: principes et utilisations potentielles en cardiologie.

Magnetocardiography (MCG) is a non-invasive technique of studying cardiac electrophysiology activity. It appears that electric and magnetic measurements are not only complementary but provide independent information. Described over 25 years ago, recent technical progress in the field of supraconductivity has provided MCG with real clinical applications. It is still mostly used in research, but its clinical applications are beginning to develop. The most interesting clinical application of the MCG is certainly its capacity to provide a non-invasive anatomical localisation of the arrhythmogenic substrate or of accessory pathways. Nowadays, however, the accuracy of these localisations needs to be improved. When this has been accomplished, MCG could play a significant role in non-invasive cardiological investigation with well-defined clinical applications.

Blood lactate concentrations during exercise: effect of sampling site and exercise mode.

BACKGROUND: The purpose of the study was to compare blood lactate concentrations determined in blood sampled from three sites (finger capillary, ear-lobe capillary, and forearm vein) during exercise on three different ergometers (a cycle ergometer, a treadmill and an arm-crank ergometer). METHODS: A total of 312 well-trained subjects performed either a six-minute steady-state exercise (n = 219) or an incremental exercise test until exhaustion (n = 93). Blood was sampled from two sites after each exercise test and at the end of each stage of the incremental protocol, 852 pairs of blood samples were analysed. RESULTS: Results showed that, when exercise was performed on a cycle ergometer or a treadmill, no significant differences between venous and ear capillary samples were observed whereas finger capillary values were higher. On an arm-crank ergometer, venous and finger capillary lactate concentrations were usually higher than ear capillary values with some discrepancies depending on the times of sampling. CONCLUSIONS: We conclude that lactate values may differ depending on the sampling site and the type of exercise mode. An ear capillary sample may be preferred because it is less affected by lactate release in the arms and easier to obtain.

Relationships between transmembrane action potential changes and simultaneous changes in electrocardiograms of rats after a one-month aortic pressure overload.

An attempt was made to determine the relationship between the characteristics of electrical activity of the hypertrophied myocardium of rats at the cellular level and at the level of the whole heart after a one-month left ventricular pressure overload. Such an animal model has already been demonstrated to be highly resistant to epinephrine-induced arrhythmias. Since severe ventricular arrhythmias often occur in patients with cardiac hypertrophy, ventricular vulnerability might depend on some electrophysiological characteristics of the heart related to the stage of hypertrophy. Using the "floating" microelectrode technique, the computed characteristics of cardiac transmembrane action potentials (AP) of the left and right epicardium cells were compared in situ to computed characteristics of the electrocardiograms in anaesthetized control rats (group C) and in rats with left ventricular hypertrophy (group H) induced by a one-month suprarenal constriction of the abdominal aorta. The aortic pressure overload caused a significant (p<0.001) and marked increase in AP duration of left ventricular cells: APD 30 and APD 80 were 29+/-3 ms and 89+/-6 ms, respectively, in group H and 14+/-1 ms and 53+/-2 ms in group C. The same modifications were observed in right ventricular cells when right hypertrophy was present. Simultaneous electrocardiograms exhibited a significant (p<0.01) prolongation of P-R, Q-S and T duration and T wave flattening in group H (63+/-2 ms, 32+/-3 ms, 109+/-5 ms and 0.25+/-0.03 mV as compared with 53+/-1 ms, 20+/-1 ms, 88+/-2 ms and 0.40+/-0.04 mV in group C). After a one-month aortic overload in rats, both left and right ventricles are hypertrophied and have the same electrophysiological characteristics: in this model, at this stage of hypertrophy, some factors favouring ventricular arrhythmias are missing. The corresponding flattening of the T wave in the ECG might be of clinical relevance.

Heart rate variability in two models of cardiac hypertrophy in rats in relation to the new molecular phenotype.

The analysis of heart rate variability (HRV) provides information on neural control of the heart. We investigated HRV in normal rats and in models of experimental cardiac hypertrophy using the Holter monitoring and peak/trough method. In normal rats, two heart rate oscillations with different wavelengths, high frequency (HF) and low frequency (LF) oscillations, were detected. The HF oscillations were insensitive to propranolol and suppressed by atropine. The LF oscillations were sensitive to both antagonists. Thyrotoxicosis resulted in cardiac hypertrophy (+20%) and tachycardia. The HF oscillations were unchanged, whereas LF oscillations were hampered at low heart rate in this group. Aortic stenosis resulted in cardiac hypertrophy (+53%), but heart rate oscillations were unchanged. The (number x amplitude) product for both types of oscillations correlated with heart rate in controls but not in the thyrotoxicosis or aortic stenosis models. Alterations of HRV in cardiac hypertrophy occur in rats as in humans. They may reflect the changes in the molecular components of the adrenergic/muscarinic system, which defines the new myocardial phenotype.

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.

Effects of captopril chronic intake on the aerobic performance and muscle strength of normotensive trained subjects.

Fifteen normotensive athletes specializing in dynamic sports took part in a randomized double-blind and cross-over study: captopril (50 mg/24 h) vs placebo. Each treatment lasted one month. Maximal exercise tests on cycle ergometer were performed at the end of each period. No significant differences were observed in the maximal values of oxygen uptake, power, heart rate or blood lactate value. The anaerobic threshold, defined as the exercise intensity which corresponded to a 4 mmol.l-1 blood lactate level was unchanged. With captopril, the end-of-exercise systolic and diastolic BP were slightly altered (NS). Lower limb muscle strength, as explored with a Cybex isokinetic system, was not modified by captopril intake. The results indicate that maximal aerobic performance and isokinetic strength of the lower limbs are not altered by captopril chronic administration (50 mg/day) in normotensive trained subjects.

Failure of epinephrine to induce severe cardiac arrhythmia in rats with ventricular hypertrophy secondary to aortic pressure overload.

The arrhythmogenic action of epinephrine was studied in 3 groups of rats: 10 rats with mild constriction of the abdominal aorta (group H1), 10 rats with severe constriction (group H2), 10 sham-operated age-matched rats (group C). Blood pressure and ECG were recorded before, during and after 5 min. perfusion of increasing doses of epinephrine (1, 5, 10 and 25 micrograms.kg-1.min.-1). Ventricular arrhythmia was evaluated from the ECG using a modified Lown's grading system. The ventricular hypertrophy index was calculated from the heart/body weight ratio (mg/g). The mean arterial blood pressure was significantly higher in groups H1 and H2 than in the control group. The ventricular hypertrophy was significant in group H2, but not in group H1. There was no significant difference between the amplitudes of the epinephrine-induced hypertensive responses in the 3 groups but the extent of arrhythmia was significantly lower in the animals with high hypertrophy index.

Extent of lactic anaerobic metabolism in handballers.

The authors investigated lactic anaerobic metabolism in handball players during practice games. Seven players aged 18-21, belonging to second division league clubs, took part in the study. In the laboratory, VO2 max and the onset of blood lactate accumulation (OBLA) were determined with progressive maximal ergocycle tests. On the field, video recordings, cardiotelemetry, and rectal temperature measurements made during the first half of the game were used to quantify exertion. An intravenous catheter worn permanently was used to draw blood for lactate measurements at the 5th, 10th, 15th, 20th, and 30th min of play and after a 10-min rest period. The results confirmed earlier observations showing the need for an excellent maximal aerobic power and capacity in handballers. However, the maximal lactate levels observed (4-9 mmol X l-1) were above those that could be expected from samples drawn only at the end of play. These findings indicate that players must be trained to tolerate high lactate levels to preserve their maximal efficiency throughout the game. Finally, lactate production increased with player exertion and with increasing OBLA.

A proposed mechanism for cardiac sensitisation: electrophysiological study of effects of difluorodichloromethane and adrenaline on different types of cardiac preparations isolated from sheep hearts.

Difluorodichloromethane (FC12) inhaled at high concentrations sensitises, as do numerous other volatile organic compounds, mammalian heart to adrenaline induced arrhythmias. In this study three types of cardiac tissue (spontaneously beating sinusal and Purkinje preparations and stimulated Purkinje fibres) were isolated from sheep hearts and perfused for electrophysiological recording to examine the effect of FC 12. Preparations were perfused alternately with a control solution of physiological fluid and a trial solution with dissolved FC 12, the partial pressure of oxygen remaining identical. Sensitisation to adrenaline was studied by injecting adrenaline at a dose causing a notable effect without producing arrhythmias in the control preparations. Examination of transmembrane potential recordings confirmed that FC 12 inhibits sinus node pacemaker stimulation by adrenaline. Conversely, the adrenaline induced acceleration of latent pacemakers in certain types of Purkinje fibres appeared to be potentialised by FC 12. The various types of arrhythmia observed in vitro were explained by the effect of FC 12 on cell membranes, an affect which can oppose or favour that of adrenaline. These phenomena explain the arrhythmias observed in isolated hearts or whole animal preparations and permit a better understanding of the mechanism involved in cardiac sensitisation to adrenaline induced arrhythmia, a mechanism in which variability in time and location is the essential factor in the FC 12 effect.

Fluorocarbons and cardiac arrhythmia: does difluorodichloromethane (FC 12) inhibit cardiac metabolism?

Certain fluorocarbons, such as difluorodichloromethane (FC 12), depress the cardiovascular system by diminution of all the transmembrane ionic conductances in cardiac tissues. Does FC 12 also inhibit active transport and thus enzymatic activity and cellular energy? We measured phosphocreatine (PC), adenosine triphosphate (ATP) and cyclic adenosine monophosphate (AMPc) in rat hearts. Rats were randomly divided into 4 groups; 2 control groups: one breathing a mixture of oxygen (21%) and nitrogen (79%) (group C) and the other breathing the same mixture but simultaneously perfused with 1 microgram/kg/min. epinephrine (groupe E-C); 2 trial groups T and E-T where nitrogen was replaced by FC 12. The maximal FC 12 concentration of 720 micrograms/ml in arterial blood produced no significant difference in the concentrations of these three metabolites compared with controls.

Mechanism of liposoluble drugs and general anaesthetic's membrane action: action of difluorodichloromethane (FC 12) on different types of cardiac fibres isolated from sheep hearts.

The effect of difluorodichloromethane (FC 12), a chemically stable aerosol propellant which has long been considered innocuous, on several types of cardiac fibres isolated from sheep hearts after preparation in a nutritive solution was studied. Modifications in resistance and transmembrane potentials suggested a mechanism of FC 12 action. Physical constraint on membrane structures produced by high FC 12 concentrations from simple dissolution in the internal lipid layer explain modifications in cardiac membrane properties. Variable effects of FC 12 with localisation and time on automatism, excitability, and conduction in various types of cardiac tissue agreed with earlier observations of the depressive and arrhythmia effect of this gas on isolated and in situ hearts.

[Effect of difluorodichloromethane (FC 12) on the cardiac cellular electric activity of mammals]. / Action du difluorodichloraméthane (FC 12) sur l'activité électrique cardiaque de mammifère au niveau cellulaire.

The cardiotoxicity of high concentrations of inhaled difluorodichloromethane (FC 12) has now been acknowledged. In the present study, the effects of FC 12 on the electrical activity of cells in the atrial and ventricular myocardium of anesthetized rats were recorded with "flexibly mounted" intracellular microelectrodes. The major phenomena observed in both types of cells were: a distinct decrease in the diastolic potential, a decrease inthe amplitude of the action potential, modifications in the shape of the action potential. Analysis of the simultaneously obtained electrocardiogram specifies the rhythm abnormalities which consist of an important decrease in the atrio-ventricular conduction and changes in the myocardial excitability. The cardiotoxicity of FC 12 is assumed to affect passive or active transmembrane ionic movements. Possible mechanisms are suggested here.

[Role of endogenous adrenaline in cardiac arrhythmia induced by dichlorodifluoromethane (FC 12) in mammals]. / Rôle de l'adrénaline endogène dans le déclenchement de l'arythmie cardiaque par le dichlorodifluorométhane (FC 12) chez les mammifères.

During the inhalation of normally oxygenated gas mixtures containing light or middle concentrations of FC 12, the presence of perfused epinephrine is necessary to induce cardiac arrhythmia in rabbits and dogs. The only inhalation of normally oxygenated gas mixtures containing a very high concentration of FC 12 produces in rabbits and dogs an important decrease in arterial pressure, tachycardia, a fall in respiratory amplitude, an acceleration reflex of respiratory frequency and cardiac arrhythmia. The same experiments in baro and chemodenervated animals show that : respiratory depression due to FC 12 still occurs, but not through the arterial chemoreceptors ; tachycardia has a reflex origin : barodenervation reveals the negative chromotropic effect of FC 12 and increases the fall in arterial pressure, mainly due to the negative inotropic effect of FC 12 ; adrenaline is necessary for FC 12-induced arrhythmia : barodenervation suppresses tachycardia due to the release of endogenous epinephrine and abolishes any arrhythmia.

[Cardiac arrhythmia in the rabbit under the effect of adrenaline and difluorodichloromethane (FC12)]. / Arythmie cardiaque chez le lapin sous l'action de l'adrénaline et du difluorodichlorométhane (FC12).

Inhalation of gas mixtures containing different concentrations of FC12 by anesthetized and normally oxygenated rabbits produces blood levels of FC12 which are stable and proportional to the rate of FC12 in the mixture. From the arterial concentration of 80 microgram/ml FC12 (10 % FC12) mixture) and over, FC12 alone causes effects proportional to doses: arterial pressure decrease with tachycardia; slight morphological alterations of the electrocardiogram at high concentration. Arrhythmia never occurs under the action of FC12 alone even at maximum arterial concentration reached here: 235 microgram/ml (40 % FC12 mixture). Recorded disturbances are always reversible. The intravenous perfusion of epinephrine alone evokes the appearance of premature contractions at only very high doses: 12 microgram/kg/min. The presence of FC12 in blood conjoined with epinephrine induces the inhibition of the hypertensive action of epinephrine at high concentrations and lowers the arrhythmogenic threshold. Both parameters interfere: the arrhythmogenic dose of epinephrine is a function of blood levels of FC12.

[Cardiac arrhythmia in dogs under the action of adrenaline and difluorodichloromethane (FC 12)]. / Arythmie cardiaque chez le Chien sous l'action de l'ardrénaline et du difluorodichlorométhane (FC 12).

Inhalation of gas mixtures containing different concentrations of FC 12 by anesthetized and normally oxygenated dogs produces blood levels of FC 12 which are stable and proportional to the rate of FC 12 in the mixture. From the arterial concentration of 40 microgram/ml FC 12 (5 % FC 12 mixture) and over, FC 12 alone causes effects proportional to doses: arterial pressure decrease with tachycardia. At high rates of FC 12 tachypnoea and slight morphological alterations of the electrocardiogram can be recorded. Arhythmia never occurs under the action of FC 12 alone even at maximum arterial concentration reached here : 230 microgram/ml (40 % FC 12 mixture). Recorded disturbances are always reversible. The intravenous perfusion of epinephrine alone evokes the appearance of premature contractions at the only dose of 5 microgram/kg/mn. The presence of FC 12 in blood conjoined with epinephrine induces the inhibition of the hypertensive action of epinephrine at high concentration and lowers the arhythmogenic threshold. The dog is clearly more sensitive than the rabbit to the arhythmogenic action of epinephrine and FC 12. The required rates of epinephrine and FC 12 validate the hypothesis of cardiac sensitization by FC 12 to the arhythmogenic action of circulating adrenaline to explain the cases of sudden "sniffing" deaths in man.

[Development of liver glycogen reserves in rats subjected to chronic alcoholic intoxication]. / Evolution des réserves de glycogène hépatique chez des rats soumis à une intoxication alcoolique chronique.

Literature offers many but very different informations about the effects of alcohol on the hepatic carbohydrates metabolism. Therefore we have tried to observe, in process of time, the evolution of the hepatic glycogen reserves on rats intoxicated by ethanol 40% during variable durations. Stuffing is made by oesophageal way at the rate of 6,4 g/kg/day. During this period of poisoning, we note a significant increasing of the hepatic glycogen reserves.

[Action of difluorodichloromethane (FC 12) and of adrenaline on the isolated rabbit heart]. / De l'action du difluorodichlorométhane (FC 12) et de l'adrénaline sur le coeur isolé de Lapin

Does difluorodichloromethane (FC 12) sensitize the cardiac muscle in vitro to epinephrine-induced arrhythmia ? We have tried to answer this question by comparing : the action of epinephrine alone on the isolated rabbit heart perfused by an ordinary nutritive solution and the action of epinephrine on the heart perfused by a nutritive solution containing various concentrations of FC 12. The results are: 1) the general action of epinephrine (inotropic and chronotropic positive effects, increase of coronary flow) is not significantly modified by the action of FC 12. 2) FC 12 does not sensitize the rabbit heart in vitro to the arrhythmogenic action of epinephrine. The few cases of arrthymia recorded under the action of adrenalin do not necessarily occur in the presence of FC 12, but rather depend on the weakened state of the preparation.