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Biomedical subjects

L Girardier

Publications and source records attributed to L Girardier.

At least 73 records · Page 4Linked to original sources
PubMed1979

alpha-Sympathetic control of glucose output of mouse liver perfused in situ.

Electrical stimulation of perivascular nerve bundles of mouse liver perfused in situ at constant flow resulted in an increase of glucose production that was maximal at 20 Hz. The neurally induced glucose output was inhibited significantly by the beta-blocker propranolol, and to a considerably greater extent by the alpha-blockers, phenoxybenzamine and phentolamine. The effect of 20-Hz electrical stimulation could be matched by an infusion of norepinephrine at a concentration of 5 X 10(-7) M. It is suggested that the carbohydrate metabolism of the liver is controlled by its own nerve supply rather than by circulating catecholamines and that alpha-adrenergic receptors have a greater effect than beta-receptors on hepatic glucose production resulting from electrical and catecholamine stimulation.

Animals↗
PubMed1978

Does cytoplasmic alkalinization trigger mitochondrial energy dissipation in the brown adipocyte?

Indirect calorimetry measurements showed that brown fat thermogenesis was very sensitive to modifications of intra-cellular pH induced by extracellular acid-base perturbations. Specific blockage of active Na-K transport by ouabain inhibited the thermogenic response only in acidosis and more efficiently when the glycoside was administered before the catecholamine stimulus than when it was added after the full calorigenic response had developed. It is suggested that the catecholamine stimulus might initiate a positive feed-back alkalinization of the cytoplasm, concomitant with activation of Na-K transport.

Adipose Tissue, Brown↗
PubMed1978

Comparative measurements of in vitro thermogenesis of brown adipose tissue from control and cold adapted rats.

Heat output and oxygen uptake rates as well as caloric equivalents of O2 were measured in brown fat fragments from cold-adapted and control rats. Resting metabolic rate per unit wet weight was the same in both groups. Submaximal responses to noradrenaline were significantly lower in the cold-adapted than in the control group. Apparent maximal responses were the same for both groups. Caloric equivalents of O2 gave no evidence for anaerobic glycolysis even under conditions of oxygen limitation.

Acclimatization↗
PubMed1978

Extrapancreatic glucagon and glucagonlike immunoreactivity in depancreatized dogs. A quantitative assessment of secretion rates and anatomical delineation of sources.

The anatomical sites and the rates of extrapancreatic secretion of glucagon and of glucagon-like immunoreactivity (GLI) were assessed in dogs 2 h after pancreatectomy by catheterization of the gastrosplenic and mesenteric veins. Glucagon release from the gastrosplenic area approximated one-fourth that of a normal pancreas and rose from 0.25 to 1.0 ng/kg per min during arginine stimulation. Intestinal glucagon secretion was small and did not respond to arginine, suggesting that the stomach is the only important extrapancreatic source of glucagon. Glucagon concentrations attained by gastrosplenic secretion were in close proportion to those obtained during the administration of exogenous glucagon, indicating similar clearance rates of extrapancreatic and pancreatic glucagon, approximating 10 ml/kg per min.GLI secretion (0.3 ng eq/kg per min) was limited to the intestinal area and was transiently stimulated by arginine and exogenous glucagon. Base-line GLI clearance approximated 1 ml/kg per min. No insulin secretion could be detected. Gastrointestinal glucose uptake rose from 0.56 to 2.2 mg/kg per min after glucagon administration suggesting that as much as 10% of total glucose production can be taken up by the gastrointestinal tract. In two dogs both the stomach and pancreas were removed. Intestinal glucagon release remained small and did not increase during arginine administration. By contrast, GLI release was stimulated by both arginine and exogenous glucagon.

Animals↗
PubMed1977

Microcalorimetric determination of energy expenditure due to active sodium-potassium transport in the soleus muscle and brown adipose tissue of the rat.

1. The resting heat production rate (E) of soleus muscles from young rats and brown adipose tissue from adult rats was measured by means of a perfusable heat flux microcalorimeter in the absence and presence of ouabain. In the soleus muscle, the acute response of E to ouabain was compared with the ouabain-suppressible components of 22Na-efflux and 42K-influx. 2. In standard Krebs-Ringer bicarbonate buffer, ouabain (10(-3)M) induced an immediate but transient decrease in E of around 5%. Both in muscle and adipose tissue this was followed by a progressive rise in heat production rate. 3. When the medium was enriched with Mg (10 mM), ouabain produced a sustained decrease in E of the same magnitude as in the standard medium and the secondary rise was less marked or abolished. Under these conditions, in the soleus muscle, ouabain inhibited E by 5% (i.e. by 1-76 +/- 0-22 mcal.g wet wt.-1.min-1), 22Na-efflux by 58% (0-187 +/- 0-013 micronmole. g wet wt.-1.min-1) and 42K-influx by 34% (0-132 +/- 0-028 micronmole. g wet wt.-1.min-1). 4. When the muscles were loaded with Na by pre-incubation in K-free Mg-enriched medium, the addition of K (3mM) induced an immediate ouabain-suppressible increase in E of 2-98 +/- 0-33 mcal. g wet wt.-1.min-1 and a concomitant stimulation of 22Na-efflux of 0-388 +/- 0-136 micronmole. g wet wt.-1.min-1. 5. Maximum Na/ATP ratios for the active Na-K transport process were computed, with no assumption as to the in vivo free energy of ATP hydrolysis. These were 2-1, 1-9 and 2-3 under the conditions described in paragraphs (2), (3) and (4) respectively. 6. The calculated reversible thermodynamic work associated with active Na-K transport corresponded to 34% of the measured ouabain-induced decrease in E. On the premise that the maximum efficiency of the cellular energy conservation processes is 65%, this estimate indicates that the minimum energetic efficiency of ATP utilization by the active Na-K transport process in mammalian muscle is 52%.

Adenosine Triphosphate↗
PubMed1976

A comparative study of the effects of norepinephrine and vasopressin on Na transport and O2 consumption in frog skin.

Experiments were designed to compare the effects of two hormones-vasopressin and norepinephrine-on the energetics of Na transport in frog skin. Simultaneous measurements of O2 consumption and net Na flux were performed in the same skins by means of O2 cathodes and the short circuit current technique. The results showed that both hormones induced similar increments in Na transport. In contrast, there was a conspicuous difference in O2 consumption values, norepinephrine having a very small stimulatory effect compared to the one induced by vasopressin. Thus, despite the fact that both hormones increase Na permeability of frog skin by similar mechanisms and to a similar extent, they appear to exert very different effects on cell metabolism.

Animals↗
PubMed1976

Control of A and B cells in vivo by sympathetic nervous input and selective hyper or hypoglycemia in dog pancreas.

An extra-corporeal blood circuit was established between the cranial pancreatico-duodenal vein and the portal vein in the dog. Timed measurements of flow, hematocrit, insulin and glucagon concentrations in this circuit were made in order to calculate the secretion rates of insulin and glucagon. The plasma glucose concentration in the pancreatico-duodenal vein was monitored at steady state from 50 to 330 mg/100 ml for periods of 70 min by infusing a saline solution or glucose into the cranio-pancreatico-duodenal artery. No change in peripheral glucose concentrations was detected. 1. When glucose concentration in the PD vein was lowered from 100 mg/100 ml to about 50 mg/100 ml, the basal insulin secretion rate was not modified. When the glucose concentration was increased from 100 mg/100 ml to about 300 mg/100 ml, the insulin secretion rate increased linearly over the range of concentrations tested. 2. Glucagon secretion rate was unmodified throughout the range of glycemia tested. Whereas net pancreatic glucagon secretion rate was not reduced by selective pancreatic hyperglycemia, it was reduced by systemic hyperglycemia at about the same concentration. 3. In atropinized pancreas, low frequency (2 Hz) electrical stimulation of the distal end of the ligated mixed pancreatic nerve caused a mean decrease of 44% in the secretion rate of insulin, and a mean increase of 42% in the secretion rate of glucagon at all PD vein glucose concentrations studied. 4. It can be concluded, therefore, that the sympathetic nervous input at physiological frequencies controls the moment-to-moment secretory activity of the A and B cells of the pancreas independently of the concentrations of glucose.

Animals↗
PubMed1975

Potassium-induced increase in oxygen consumption of brown adipose tissue from the rat.

1. In brown adipose tissue, noradrenaline induces an increase in respiration and a depolarization of the cells. The effect of an increase in potassium concentration in a range known to depolarize the brown adipocytes was tested on the O2 consumption. 2. Isolated interscapular brown adipose tissue from the rat was incubated in chambers that allowed O2 consumption to be measured over prolonged periods. 3. 45-50 mM-KC1 were found to induce a more that fourfold increase in O2 consumption, which was stable, reversible and dependent upon the presence of calcium in the meduim. 4. When rats were pre-treated with reserpine or 6-hydroxydopamine the KC1-induced increase in O2 consumption was sharply reduced or entirely adsent. 5. The effect of KC1 was greatly inhibited by (-)-propranolol, but not by (+)-propranolol. 6. Moderate increases in O2 consumption induced by low concentrations of potassium were potentiated by desipramine, a drug which is known to block the uptake of catecholamines by adrenergic nerve endings. 7. Surgical denervation caused a decrease in the catecholamine content of the tissue, but had no effect on the KC1 response. 8. It is concluded that in brown adipose tissue, potassium stimulates O2 consumption by causing a release of noradrenaline from nerve endings. This implies that surgical denervation as it is commonly performed on this tissue does not denervate the brown adipocytes but probably only the blood vessels.

Adipose Tissue, Brown↗
PubMed1973

Neural regulation of insulin secretion in the dog.

The effects of stimulation of the mixed autonomic nerve to the dog pancreas has been studied under conditions in which both pancreaticoduodenal vein blood flow and insulin concentration were determined. Stimulation resulted in increased insulin output, which was blocked by prior administration of atropine. Blood flow was reduced by stimulation in proportion to the rate of stimulation. At 40 stimuli/s a maximum effect was found at 1 min with a gradual return toward base line despite continued application of the stimulus. Atropinization had no effect on blood flow changes. Insulin responses to 0.1 g/kg glucose were reduced on the average 40% by simultaneous stimulation of the pancreatic nerve at 40 cycles/s in atropinized animals. These studies establish this preparation as a reproducible model for the direct examination of autonomic influences on endocrine pancreatic function. From them it is concluded that the nerve supply to the endocrine pancreas of the dog is sufficient to inhibit insulin secretion by activation of the sympathetic nerves and to stimulate insulin secretion by activation of the parasympathetic nerves.

Animals↗
PubMed1973

Glucagon release induced by pancreatic nerve stimulation in the dog.

A direct neural role in the regulation of immunoreactive glucagon (IRG) secretion has been investigated during stimulation of mixed autonomic nerves to the pancreas in anesthetized dogs. The responses were evaluated by measurement of blood flow and hormone concentration in the venous effluent from the stimulated region of pancreas. Electrical stimulation of the distal end of the discrete bundles of nerve fibers isolated along the superior pancreaticoduodenal artery was invariably followed by an increase in IRG output. With 10-min periods of nerve stimulation, the integrated response showed that the higher the control glucagon output, the greater was the increment. Atropinization did not influence the response to stimulation. That the preparation behaved in physiologic fashion was confirmed by a fall in IRG output, and a rise in immunoreactive insulin (IRI) output, during hyperglycemia induced by intravenous glucose (0.1 g/kg). The kinetics of this glucose effect on IRG showed characteristics opposite to those of nerve stimulation: the lower the control output, the less the decrement. Furthermore, during the control steady state, blood glucose concentration was tightly correlated with the IRI/IRG molar output ratio, the function relating the two parameters being markedly nonlinear. Injection or primed infusion of glucose diminished the IRG response to simultaneous nerve stimulation. Measurement of IRG was inferred to reflect response of pancreatic glucagon secretion on the basis of the site of sample collection (the superior pancreaticoduodenal vein), the absence of changes in arterial IRG, and similar responses being obtained using an antibody specific for pancreatic glucagon. THESE STUDIES SUPPORT A ROLE FOR THE AUTONOMIC NERVOUS SYSTEM IN THE CONTROL OF GLUCAGON SECRETION: direct nerve stimulation induces glucagon release. Such sympathetic activation may be interpreted as capable of shifting the sensitivity of the A cell to glucose in the direction of higher glycemia for a given glucagon output. The experimental model employed is valid for further studies of regulatory mechanisms of endocrine pancreatic function in vivo.

Animals↗