Archives internationales de physiologie et de biochimie最新文献

The influence of neonatal hypo- and hyperthyroidism on different aspects of tyrosine metabolism in the hypothalamus, striatum, brainstem, adrenal glands, heart and brown adipose tissue (BAT) were studied in 14-day old rats. The synthesis rate of catecholamines (CA) was also determined in vivo after the injection of labelled tyrosine. Hypothyroidism increases tyrosinaemia and endogenous tyrosine concentration in the hypothalamus and BAT. Hyperthyroidism decreases tyrosinaemia and endogenous tyrosine levels in the striatum, adrenals and heart. The accumulation rate of tyrosine determined 30 min after an intravenous injection of the labelled amino acid has been determined in the organs, together with the influx of the amino acid, determined within 20s. Hypothyroidism increases tyrosine accumulation rate in all the organs studied, and tyrosine clearance is decreased in the striatum and brainstem; together with an increased tyrosinaemia, this leads to a normal influx. The influx of tyrosine is increased in the hypothalamus. Hyperthyroidism decreases tyrosine accumulation rate in all the organs except the adrenals. These results indicate that the thyroid status of the young rat can influence tyrosine uptake mechanisms, without modifying an organ's tyrosine content. The fact that hypothyroidism increases tyrosine influx in the hypothalamus without modifying it in the brainstem and striatum reflects an heterogeneous reactivity to the lack of thyroid hormones in different brain structures. Neonatal hypothyroidism decreases the CA synthesis rate in the striatum, the heart and the interscapular brown adipose tissue, while synthesis was enhanced in the brainstem and the adrenals. It is likely that these variations in CA synthesis are due to thyroid hormone modulation of tyrosine hydroxylase activity, the enzyme which catalyses the rate limiting step in CA biosynthesis.

When exposed to hypoxia, the isolated rat atria released lactate into the bathing medium and underwent a rise in resting tension and a decline of the contractions frequency. In some of them, it also occurred a complete cessation of the pacemaker activity. Atria from 24-h fasted rats, when compared to those from fed ones, exhibited a lower lactate output, a higher rise in resting tension, a faster decay of the contraction frequency and an increased occurrence of atrial arrest. In both the fed and fasted rats atria, some triacylglycerol lipolysis remained throughout the hypoxic incubation. Addition of 2 mM 4-pentenoic acid abolished the lipolytic activity and reduced lactate output in both groups of atria. In the fed rats atria it also accelerated the decrease of the pacemaker frequency. Pentanoic acid reduced lactate output in both groups of atria and in those from fed rats it did not alter lipolysis but increased the rise in resting tension, the decline of the pacemaker frequency and the occurrence of atrial arrest. Present data indicate that although 4-pentenoic acid inhibits fatty acid oxidation and endogenous lipolysis, it was not able to reduce the noxious effects of hypoxia. Since the effects of 4-pentenoic acid were rather similar to those of fasting and pentanoic acid, they might be ascribed to the accumulation of its own oxidative metabolites which could be detrimental for the hypoxic atria.

The cardiovascular responses of rats anaesthetised with different anaesthetic agents to acute coronary artery ligation were studied. Before thoracotomy, urethane-anaesthetised animals exhibited significantly lower blood pressures. Ligation of the left coronary artery induced a high incidence of ventricular tachycardia or fibrillation in rats anaesthetised with pentobarbitone, urethane, or ether inhalation followed by chloralose. Ketamine-anaesthetised animals had a significantly lower incidence of ventricular arrhythmias. The mortality rate was also lower, though not statistically significant. However, all groups of rats showed essentially similar blood pressure and heart rate changes following coronary artery ligation as well as the time of onset of ventricular tachycardia or fibrillation. The findings demonstrate the influence of anaesthetics on the occurrence of early ventricular arrhythmias following acute coronary artery ligation in rats.

Effects of pirenzepine, known as a muscarinic receptor antagonist, on the contraction of dog gallbladder elicited by cholecystokinin (CCK) were examined in comparison with atropine and hexamethonium ones. Intraluminal gallbladder pressure in an in situ anaesthetized dog model was chosen for studying gallbladder motility. The intravenous administration of pirenzepine (0.75 mg/kg b.wt.), atropine (3 mg/kg b.wt.) or hexamethonium (5 mg/kg b.wt.) elicited a marked decrease in the increase of intraluminal gallbladder pressure induced by intravenous bolus injections of CCK (0.25-2 Ivy dog unit/kg b.wt.) and by continuous infusion of CCK (0.025-0.4 Ivy dog unit/kg b.wt./min). It was concluded that CCK induced gallbladder contractions were influenced by both nicotinic and muscarinic receptors.

Metabolic impairment in skeletal muscle was suggested to be involved in the development of local mechanical fatigue but until now results have dealt with short activity periods whereas little data on exhaustive and prolonged exercises are available. Stimulations of rat leg muscle lasting 45 min were induced by tetanic trains delivered via sciatic nerve at five different rhythms. Energy metabolism of the stimulated gastrocnemius muscle was followed by 31P NMR spectroscopy using surface coil while mechanical function was recorded. Our data showed a decrease in the force level to very low values a few minutes after exercise onset. This mechanical impairment only induced a transient metabolic failure followed by rapid restoration of high phosphocreatine (PCr) values and intracellular pH, without mechanical recovery. In addition, at the end of exercise, the PCr content was proportional to the fatigue level. As these experiments could not have impaired neuromuscular junction, the data would indicate that fatigue was maintained by a mechanism which does not appear to depend directly on muscle cell energy stores.

The kinetics of the low-Km hexokinase isoenzymes, which obey the Michaelis-Menten equation, can be established from the Km (Michaelis constant) and Vmax (maximal velocity) values for either equilibrated D-glucose or its alpha- and beta-anomers. In the case of the high-Km glucokinase isoenzyme, however, the sigmoidal substrate dependency and the competition between the two anomers of D-glucose do not allow, theoretically, to assign any meaningful value to either the Km, Vmax or n (Hill number) constants for equilibrated D-glucose. Thus, with equilibrated D-glucose, the concentration dependency fails to display a rectilinear relationship in the Hill plot. These observations illustrate the shortcomings of current biochemical studies in which the anomeric heterogeneity of D-glucose is ignored.

The action potential is a dissipative process producing entropy and using free energy. This is well demonstrated by: 1) the evolution of the Na conductance under voltage clamping conditions, 2) the microcalorimetric measurements, 3) the analysis of heat evolution during the conductance changes. The most appropriate explanation must involve an exogenous energy source since the energy dissipated by the ionic flows or even the applied stimulus depolarization are far too small to account for the overall energy balance. Thiamine triphosphate is a likely candidate as specific operating substance. The more so, since it is specifically hydrolyzed by a triphosphatase the activity of which is modulated by various anions. It is therefore suggested that the control of the Cl-permeability, a process requiring the hydrolysis of thiamine triphosphate, is the key to our understanding of the energetics of the action potential.

Highest Mg concentration in whole intermoult, 7th growth-stage Porcellio spinicornis, exposed for 7 days to various Mg [367.39 ppb (carrot powder-control), 217.6 ppb (apple powder-control), 100, 150, 500, and 1000 ppm Mg, as well as two mixtures containing 500 ppm Mn + 150 ppm Mg and 500 ppm Mg + 500 ppm Mn)], and Mn concentrations [97.9 ppb (carrot powder-control), 2.0 ppb (apple powder-control), 100, 150, 500 and 1000 ppm)], was observed in males feeding on 500 ppm Mn + 150 ppm Mg, and lowest in females on 500 ppm dietary Mg. Highest tissue Mn concentration, on the other hand, was observed in males exposed to 1000 ppm dietary Mn, and lowest in females on 500 ppm Mg. Approximately 42% of the total tissue Mg was present in hepatopancreas and the remaining in other body tissues, including exoskeleton. In contrast, 78.55% Mn was stored in hepatopancreas and 21.4% in remaining body tissues. Differences between hepatopancreatic Mg levels were not significant between the two sexes, but differences in Mn levels between males and females were significant at P less than 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)