Search PubMed⌕ Search

Biomedical subjects

M Paillard

Publications and source records attributed to M Paillard.

At least 91 records · Page 5Linked to original sources
PubMed1990

Does the stress of admission to an intensive care unit influence arginine vasopressin secretion and renal diluting ability?

The pathogenesis of excessive arginine vasopressin (AVP) release and hyponatraemia in euvolaemic intensive care unit (ICU) patients is poorly understood. Stress has frequently been proposed as a possible determinant, but its actual responsibility has not been adequately assessed. Therefore, water-load tests were prospectively performed in 11 patients admitted to the ICU for severe or potentially severe diseases, but who had no other condition which could result in excessive AVP release or impairment of renal diluting ability. Renal diluting ability was normal in 9 patients. Two patients exhibited very slight defects, which might be the consequence of subclinical haemodynamic alterations, since one had a pulmonary embolism and the other manifested a gastrointestinal haemorrhage just after the completion of the water load. Nevertheless, plasma AVP levels decreased in response to the water load in all the patients, resulting in a significant decrease in mean values. Plasma norepinephrine values were found to be elevated both before and after water loading. A highly significant correlation existed between the levels of norepinephrine and those of AVP measured before the load, but was lost after it. In addition, norepinephrine values were markedly elevated in two patients who exhibited strictly normal renal diluting abilities, and no correlation was found between plasma norepinephrine values and any parameter of renal water excretion. Our study shows that the stress of a serious illness and of admission to an ICU does not seem to interfere, by itself, with osmotic regulation of AVP secretion and renal diluting ability, and that sympathetic activation is not, under such circumstances, a predominant stimulus for AVP release.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Acute metabolic acidosis enhances circulating parathyroid hormone, which contributes to the renal response against acidosis in the rat.

Acute PTH administration enhances final urine acidification in the rat. HCl was infused during 3 h in rats to determine the parathyroid and renal responses to acute metabolic acidosis. Serum immunoreactive PTH (iPTH) concentration significantly increased and nephrogenous adenosine 3H,5H-cyclic monophosphate tended to increase during HCl loading in intact and adrenalectomized (ADX) rats despite significant increments in plasma ionized calcium. Strong linear relationships existed between serum iPTH concentration and arterial bicarbonate or proton concentration (P less than 0.0001). Serum iPth concentration and NcAMP remained stable in intact time-control rats and decreased in CaCl2-infused, nonacidotic animals. Urinary acidification was markedly reduced in parathyroidectomized (PTX) as compared with intact rats during both basal and acidosis states; human PTH-(1-34) infusion in PTX rats restored in a dose-dependent manner the ability of the kidney to acidify the urine and excrete net acid. Acidosis-induced increase in urinary net acid excretion was observed in intact, PTX, and ADX, but not in ADX-thyroparathyroidectomized rats. We conclude that (a) acute metabolic acidosis enhances circulating PTH activity, and (b) PTH markedly contributes to the renal response against acute metabolic acidosis by enhancing urinary acidification.

Acidosis↗
PubMed1989

[Metabolism of calcium and phosphorus].

More than 99 p. 100 of calcium and 90 p. 100 of phosphorus are located in the bone tissue in the form of hydroxy-apatite crystals. Plasma ionized calcium is very tightly regulated, in order to stabilize the membranes of excitable cells, such as nerve and muscle. The PTH-1,25 (OH)2 D axis, triggered by very small variations in plasma ionized calcium (negative feedback) is the major control system of intestinal absorption, movements between bone cells and extracellular fluid, and tubular reabsorption of calcium by the kidney. Thus, usual variations in dietary intake induced no detectable change in plasma calcium and only small variations in 24 h-urinary calcium excretion rate. Plasma phosphate fluctuates over 24h-periods, and homeostatic mechanisms seem to control the concentration and/or content of phosphate in soft tissue cells (phosphate is necessary to ATP-synthesis and phosphorylation of intermediate metabolites). The PTH-1,25 (OH)2D axis which is not triggered by variations in plasma phosphate, does not control tightly intestinal absorption, movements between bone cells and extracellular fluid, or tubular reabsorption of phosphate by the kidney. However, the phosphate reabsorption in the proximal tubule of the kidney is rigidly adjusted to the phosphate available in the digestive lumen and the phosphate needs of soft tissue cells, probably via as yet undetermined factor(s). Thus, usual variations in dietary phosphate intake influence notably the plasma concentration and 24 h-urinary excretion rate.

Adaptation, Physiological↗
PubMed1989

Peptide hormone effects on urinary acidification and acid-base balance: PTH, ADH, and glucagon.

That the adaptation of the kidney to the acid-base status may be controlled by peptide hormones is considered. In the proximal tubule parathyroid hormone (PTH) inhibits reabsorption of both bicarbonate and phosphate. The former effect is compensated for by an increase in bicarbonate absorption in Henle's loop, and the latter effect serves to augment phosphate concentration in the distal tubular fluid, which stimulates proton secretion in collecting ducts, the net effect of PTH administration being an enhancement of urinary acidification. In the thick ascending limb, both antidiuretic hormone (ADH) and glucagon inhibit bicarbonate absorption. In distal and cortical collecting tubules ADH stimulates net bicarbonate absorption and glucagon net bicarbonate secretion, which results in stimulation and inhibition of final urine acidification, respectively. Acute acid loading stimulates endogenous PTH secretion, which, by enhancing urinary acidification, constitutes a homeostatic response of the parathyroid glands. The major effects of ADH on urinary acidification serve at least to counterbalance disturbing consequences on urinary ammonia excretion of physiological variations in the urinary flow rate. The physiological significance of the effects of glucagon is unclear at present. Thus other peptide hormones may add to PTH and corticosteroid hormones to modulate urinary acidification, which leads to the concept of a pluri-hormonal control of acid-base balance.

Acid-Base Equilibrium↗
PubMed1989

Effects of glucagon on H(+)-HCO3- transport in Henle's loop, distal tubule, and collecting ducts in the rat.

Paired micropuncture experiments were carried out in somatostatin-infused volume-expanded rats to examine the effects of a glucagon infusion (0.05 ng.min-1.g body wt-1) on urinary acidification and tubular handling of bicarbonate. Whole kidney and single-nephron glomerular filtration rate were not affected by glucagon. In thyroparathyroidectomized (TPTX) rats, glucagon inhibited the reabsorption of total CO2 in Henle's loop. In intact animals, however, the latter effect was not observed. In the distal tubule accessible to micropuncture, net total CO2 absorption was observed during volume expansion plus somatostatin infusion, which reversed to net total CO2 secretion during glucagon infusion in Wistar rats; thus the late distal delivery of total CO2 increased almost 80%. Marked inhibition of urinary acidification occurred in all animals as evidenced by a rise in urine pH and bicarbonate excretion. Conversely, a somatostatin infusion, which decreased the plasma glucagon concentration, stimulated net total CO2 absorption along the distal tubule and augmented final urine acidification in Wistar rats. Finally, urine-minus-blood PCO2 during alkaline diuresis was significantly reduced by glucagon infusion in bicarbonate-loaded TPTX rats. We conclude that 1) glucagon inhibits bicarbonate absorption in superficial Henle's loop in TPTX but not in intact rats, and 2) glucagon stimulates bicarbonate secretion and/or inhibits proton secretion in the distal tubule and collecting ducts, which leads to reduced urinary acidification.

Animals↗
PubMed1989

Determinants of parathormone secretion in primary hyperparathyroidism.

We studied the effects of acute modifications in plasma calcium on parathormone (PTH) secretion in 23 patients with primary hyperparathyroidism (PHPT). In 12 patients, PTH hypersecretion was autonomous, and basal plasma calcium concentration was positively correlated with maximal serum PTH(1-84) reached during Na2EDTA infusions. In 11 patients, PTH hypersecretion remained suppressible, but with elevated set point value, and basal plasma calcium concentration was positively correlated with set point. Thus, the degree of hypercalcemia seems mainly determined by the magnitude of maximal PTH secretion and set point error in autonomous and suppressible PHPT, respectively. We have previously suggested that high serum calcitriol levels might chronically inhibit PTH hypersecretion in PHPT. We showed that hyperparathyroid patients with renal stone presentation exhibited an abnormally high value of circulating calcitriol and a moderately elevated PTH activity, while patients with severe bone disease presentation displayed a low to normal calcitriol value and a dramatically increased PTH activity. The hypothesis was supported by a recent study from our Unit in one hyperparathyroid patient with severe bone disease and normal serum calcitriol level. Increment of serum calcitriol after daily intravenous Rocaltrol for 5 days directly suppressed PTH hypersecretion without change in plasma ionized calcium.

Calcitriol↗
PubMed1989

[Metabolic investigation of calcium renal lithiasis in adults and therapeutic advice].

The various lithogenic factors are analysed. In patients with calculi it is proposed that the following are systematically carried out: -- precise analysis of the calculus even if this contains calcium to separate oxalate calculi from phosphate and carbonate calculi; -- plasma calcium, phosphate and uric acid levels together with electrolytes; -- 24 hour urine samples, on a normal diet, for calcium, creatinine, protein, phosphate, oxalate and citrate levels. Depending on the results obtained, further biological investigations may be carried out or certain aspects of the history investigated in more detail. In fact, it is essentially dietary factors which enable prevention: adequate fluid intake and normalisation of calcium, protein and sodium in take in response to laboratory abnormalities. Drug therapy is only justified in patients with recurrent calculi.

Calcium↗
PubMed1989

Marked direct suppression of primary hyperparathyroidism with osteitis fibrosa cystica by intravenous administration of 1,25-dihydroxycholecalciferol.

A marked direct suppression of primary hyperparathyroidism with osteitis fibrosa cystica has been achieved by the intravenous administration of 1,25-dihydroxycholecalciferol [1,25(OH)2D]. In a recent survey of 306 patients with primary hyperparathyroidism (PHPT), we hypothesized that the far higher degree of parathyroid hormone (PTH) hypersecretion in PHPT with osteitis fibrosa cystica than in PHPT without overt bone disease might be due to the absence of suppression of hormonal hypersecretion by the low-to-normal circulating 1,25(OH)2D reflecting a relative vitamin D deficiency. To test this hypothesis, a patient having hypercalcemic PHPT with florid osteitis fibrosa cystica and normal serum 1,25(OH)2D was given increasing daily doses of intravenous calcitriol (0.5-2 micrograms) for several days. Doubling the level of circulating 1,25(OH)2D from 48 to 100-114 pg/ml was accompanied by a marked decline (46%) in serum iPTH(1-84), without a change in the serum calcium concentration. A lowered set point of parathyroid cells for calcium, and a diminished maximum secretory rate of PTH, may contribute to the marked suppression of PHPT.

Calcitriol↗
PubMed1989

Effects of citrate on urinary calcium excretion.

Thyroparathyroidectomized rats were studied during control, citrate infusion, and recovery periods to analyze the effects of citrate on urinary calcium excretion. The rats were infused with human PTH-(1-34) at a constant rate throughout the experiments that produced physiologic circulating PTH activity. Ultrafiltrable calcium was measured with a micropartition system while maintaining constant the pH and PCO2 of the sample. The plasma acid-base status, filtered load of calcium, and urinary sodium excretion rate did not vary during citrate infusion. The urinary calcium excretion rate increased from 71 +/- 9 nmol/min/g kidney during control period to 122 +/- 22 nmol/min/g kidney (p less than 0.05) during citrate infusion, and then returned below control levels during recovery period. A strong positive linear relationship was observed between the urinary excretion rates of calcium and citrate (r = 0.88; p less than 0.001). We conclude that tubular fluid citrate inhibits renal calcium reabsorption probably by forming calcium-citrate complexes.

Animals↗
PubMed1988

Factors associated with early remission of type I diabetes in children treated with cyclosporine.

To improve criteria for entry into future trials of immunosuppression, we enrolled 40 children with recent-onset Type I insulin-dependent diabetes in a pilot trial of cyclosporine. Twenty-seven patients were able to discontinue insulin therapy 48 +/- 5 days after the start of immunosuppression. At four months, their fasting and postprandial blood glucose concentrations averaged 110 and 160 mg per deciliter (6.1 and 8.9 mmol per liter) with a mean hemoglobin A1c level of 6.15 percent. Seventy-five percent of these patients with early remission still did not need insulin at 12 months, and their glycemic control was similar to that at 4 months. The major differences between the 27 patients with remission and the 13 without remission were the duration of symptoms before diagnosis (26.8 vs. 48.0 days, P less than 0.01), the degree of weight loss (3.2 vs. 10 percent of body weight, P less than 0.001), the initial hemoglobin A1c level (10.7 vs. 13.2 percent, P less than 0.001), and the frequency of ketoacidosis (11 vs. 61.5 percent, P less than 0.001). The lesser degree of weight loss was the strongest independent predictor of remission. The response of C-peptide to intravenous glucagon (0.50 vs. 0.17 pmol per milliliter, P less than 0.05) was also an independent predictor. No differences were observed between the two groups of patients in age, sex, HLA phenotype, autoantibodies to insulin or islet-cell antigens, or doses or trough levels of cyclosporine. Only minimal manifestations of toxicity were detected over the period of observation. We conclude that early treatment with cyclosporine in children with recent-onset Type I diabetes can induce remission from insulin dependence, with half the patients not requiring insulin after a full year.

Adolescent↗
PubMed1988

Glucagon inhibits urinary acidification in the rat.

The effects on urinary acidification of an acute infusion of glucagon (GLU) were studied by paired experiments in plasma-replete rats whose endogenous GLU secretion was restrained by a 0.7 ng.min-1.g body wt-1 somatostatin infusion. GLU did not affect the glomerular filtration rate in any of the plasma-replete rats studied. In 10 thyroparathyroidectomized (TPTX) rats and five intact rats subjected to hypotonic volume expansion, a low-dose (0.02 ng.min-1.g body wt-1) GLU infusion that raised the plasma GLU concentration from 302 +/- 63 to 1,010 +/- 140 pg/ml significantly increased the urinary bicarbonate excretion and decreased the urinary net acid excretion; a high-dose (0.05 ng.min-1.g body wt-1) glucagon infusion in the intact rats, that increased the plasma GLU concentration to 1,609 +/- 307 pg/ml, further enhanced the urinary bicarbonate excretion rate. In intact plasma-replete rats that were not subjected to a hypotonic volume expansion, low- and high-dose GLU infusions failed to affect the urinary bicarbonate excretion rate. Finally, no change in urinary excretion rates was noted in TPTX volume-expanded time control rats. We conclude that 1) physiological increments in plasma GLU concentration decrease urinary acidification by affecting the tubular H+/bicarbonate transport; 2) the bicarbonaturic effect of GLU may be blunted by the renal effects of high circulating antidiuretic hormone levels, or may be facilitated in an undetermined manner by hypotonic volume expansion.

Animals↗
PubMed1988

Acute infectious pneumonia is accompanied by a latent vasopressin-dependent impairment of renal water excretion.

The mechanism of hyponatremia associated with pneumonia has not been definitely established. Moreover, renal water excretion was never systematically investigated in cases of pneumonia without hyponatremia. We therefore studied nine consecutive patients breathing spontaneously (nasal oxygen in five), with acute infectious pneumonia and normal plasma sodium concentration. All the patients were previously healthy. Water loads were administered during illness and after recovery. Extracellular fluid volume, arterial blood pressure, PaO2, and PaCO2 were identical during and after pneumonia. By contrast, renal water excretion was markedly impaired during pneumonia and returned to normal values after recovery. This was attested to by a significant decrease in minimum urine osmolality together with significant increases in the percentage of the excreted water load and the maximum free water clearance, after resolution of the pneumonia. Plasma arginine vasopressin values were significantly higher during pneumonia than after recovery despite similar plasma sodium concentrations, both before and after water load. A positive correlation between plasma arginine vasopressin and minimum urine osmolality was found during pneumonia. Thus, impairment in renal water excretion appeared to be due to resetting of the vasopressin osmostat and could not be attributed to any recognized nonosmotic stimulus for vasopressin secretion. On the other hand, these defects varied in severity depending on the extent of the pneumonia and persisted until clearing of alveolar opacities, accounting for their protracted course in some patients. We conclude that water excretion is impaired in most if not in all patients with acute infectious pneumonia (especially if extended), and that the administration of hypotonic solutions should be avoided in these patients.

Acute Disease↗
PubMed1988

Maximal PTH secretory rate and set point for calcium in normal subjects and patients with primary hyperparathyroidism. In vivo studies.

The characteristics of PTH secretion, which have been extensively studied in vitro with dispersed cells of normal and abnormal parathyroid glands, remain poorly studied in vivo. We performed ethylenediamine tetraacetate (EDTA) intravenous infusions in 12 normal subjects and 5 patients with hypercalcemia (serum ionized calcium between 2.72 and 2.89 mEq/l) and surgically proven primary hyperparathyroidism (PHPT) to establish the relationship between nephrogenous cyclic AMP (NcAMP) used as an index of PTH secretion and serum ionized calcium. We determined the maximal NcAMP taken as an index of maximal secretory rate for PTH, the set point and sensitivity of parathyroid cells for calcium. In normal subjects, mean values (+/- SD) were 4.04 +/- 0.47 nmol/dl glomerular filtrate (GF) for maximal NcAMP, 2.23 +/- 0.04 mEq/l for set point, and -250 +/- 58 for sensitivity when NcAMP was expressed in percent of maximal value and serum calcium in mEq/l. In patients with PHPT, the differences between maximal and basal values of NcAMP represented 50% or more of maximal NcAMP, indicating that PTH secretion was suppressible. Sensitivity values were within normal limits in all patients. Calculated set point values were abnormally elevated (between 2.64 and 2.83 mEq/l) in all patients. Maximal NcAMP values ranged from low to normal (2.77 nmol/dl GF) to abnormally high (6.64 nmol/dl GF), and a positive linear correlation was observed with parathyroid cell mass. Basal serum calcium concentrations were not correlated with either parathyroid cell mass or maximal NcAMP values, and were close to calculated set point values for each patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Renal mass and reserve of vitamin D: determinants in primary hyperparathyroidism.

We studied circulating 1,25(OH)2D3 and its determinants in 102 patients with primary hyperparathyroidism (PHPT), 33 of them with recurrent renal stones, 60 with non-specific symptoms, and nine with overt bone disease. Means for serum 1,25(OH)2D3 and intestinal absorption of calcium were abnormally high in the renal stone group, slightly elevated in the non-specific group, and low-normal in the bone disease group. In the whole population of patients, we found a positive correlation between circulating 1,25(OH)2D3 and creatinine clearance (taken as an index of the functional renal mass). Negative correlations were observed between 1,25(OH)2D3 and age, and between creatinine clearance and age, the latter being not different from that observed in a normal large population. In the renal stone group, means for the determinants of the renal 1 alpha hydroxylase activity, that is, PTH activity expressed as nephrogenous cyclic AMP (NcAMP), serum phosphate and calcium were identical to those of the group with non-specific symptoms. However means for age were lower and functional renal mass significantly higher in the renal stone group, which may account for the higher value of circulating 1,25(OH)2D3. In the bone disease group, means for age, renal mass and serum calcium were identical to those of the group with non-specific symptoms, and NcAMP was far higher and hypophosphatemia more marked, which may not account for the lower value of circulating 1,25(OH)2D3. However, in the bone disease group, serum 25(OH)D was abnormally low, which may limit the renal production of 1,25(OH)2D3 and explain the low-normal circulating values.(ABSTRACT TRUNCATED AT 250 WORDS)

Bone Diseases↗