Biomedical subjects

F Leviel

Publications and source records attributed to F Leviel.

36 records · Page 2Linked to original sources

PubMed1987

Hemodynamic, gas exchange, and hormonal consequences of LBPP during PEEP ventilation.

Hemodynamic, gas exchange, and hormonal response induced by application of a 25- to 40-mmHg lower body positive pressure (LBPP), during positive end-expiratory pressure (PEEP; 14 +/- 2.5 cmH2O) were studied in nine patients with acute respiratory failure. Compared with PEEP alone, LBPP increased cardiac index (CI) from 3.57 to 4.76 l X min-1 X m-2 (P less than 0.001) in relation to changes in right atrial pressure (RAP) (11 to 16 mmHg; P less than 0.01). Cardiopulmonary blood volume (CPBV) measured in five patients increased during LBPP from 546 +/- 126 to 664 +/- 150 ml (P less than 0.01), with a positive linear relationship between changes in RAP and CPBV (r = 0.88; P less than 0.001). Venous admixture (Qva/QT) decreased with PEEP from 24 to 16% (P less than 0.001) but did not change with LBPP despite the large increase in CI, leading to a marked O2 availability increase (P less than 0.001). Although PEEP induced a significant rise in plasma norepinephrine level (NE) (from 838 +/- 97 to 1008 +/- 139 pg/ml; P less than 0.05), NE was significantly decreased by LBPP to control level (from 1,008 +/- 139 to 794 +/- 124 pg/ml; P less than 0.003). Plasma epinephrine levels were not influenced by PEEP or LBPP. Changes of plasma renin activity (PRA) paralleled those of NE. No change in plasma arginine vasopressin (AVP) was recorded. We concluded that LBPP increases venous return and CPBV and counteracts hemodynamic effects of PEEP ventilation, without significant change in Qva/QT. Mechanical ventilation with PEEP stimulates sympathetic activity and PRA apparently by a reflex neuronal mechanism, at least partially inhibited by the loading of cardiopulmonary low-pressure reflex and high-pressure baroreflex. Finally, AVP does not appear to be involved in the acute cardiovascular adaptation to PEEP.

Adult↗

PubMed1987

Effects of antidiuretic hormone on urinary acidification and on tubular handling of bicarbonate in the rat.

Paired micropuncture experiments were carried out in plasma-replete volume-expanded rats to examine the acute effects of 1-desamino-8-D-arginine vasopressin (dDAVP) on urinary acidification and tubular handling of bicarbonate and chloride. No effect was detected on the fractional absorption of water, total CO2, and chloride at end-proximal and early distal sites of superficial nephrons in intact animals; dDAVP, however, inhibited the fractional absorption of total CO2 in Henle's loop while stimulating that of chloride in thyroparathyroidectomized (TPTX) somatostatin-infused rats. In the distal tubule accessible to micropuncture, net total CO2 secretion was observed during hypotonic volume expansion, which reversed to net total CO2 absorption during dDAVP infusion in intact Wistar rats. Marked stimulation of urinary acidification occurred in all animals as attested by a fall in urine pH and bicarbonate excretion. Net acid excretion almost doubled in intact rats. We conclude that (a) antidiuretic hormone (ADH) inhibits fractional bicarbonate absorption in the thick ascending limb while stimulating that of chloride at least in TPTX somatostatin-infused rats, and (b) ADH stimulates proton secretion (or inhibits bicarbonate secretion) in the distal tubule and cortical collecting ducts, which leads to enhanced urinary acidification.

Acids↗

PubMed1986

Effects of increase in plasma calcium concentration on renal handling of NaCl and NaHCO3.

Recollection micropuncture experiments were carried out in thyroparathyroidectomized volume-expanded rats to examine the effects of CaCl2 infusion on the renal and nephronal segmental handling of chloride and bicarbonate. In group 1A, a 0.23 mM increase in plasma calcium concentration [delta(Ca)P] reduced urinary total CO2 (tCO2) excretion from 401 +/- 90 to 166 +/- 43 nmol X min-1 X g kidney wt-1 (P less than 0.05), whereas tCO2 filtered load was slightly diminished from 34,086 +/- 3,627 to 28,904 +/- 2,496 nmol X min-1 X g kidney wt-1 (NS). In group 1B [delta(Ca)P, 0.73 mM], whole kidney filtered loads were significantly lowered, as was urinary tCO2 excretion; however, urinary excretion of sodium, chloride, and water remained constant. Calcium infusion inhibited the proximal reabsorption of chloride 25% and water 16%; however, calcium infusion caused the end-proximal tCO2 concentration to significantly decrease so that the absolute and fractional tCO2 reabsorption remained constant. In group 2 [delta(Ca)P, 0.43 mM], whole kidney filtered load was unchanged for chloride and water but decreased for bicarbonate; urinary tCO2 excretion was reduced, whereas chloride and water excretion increased. In this group, early distal micropunctures evidenced that superficial single-nephron filtered loads were significantly reduced during calcium infusion; early distal chloride delivery was enhanced from 348 +/- 32 to 441 +/- 36 pmol X min-1 X g kidney wt-1 (P less than 0.05), whereas tCO2 delivery decreased from 47 +/- 5 to 38 +/- 4 pmol X min-1 X g kidney wt-1 (P less than 0.05). In group 3 of time control animals, whole kidney and early distal data were unchanged during second period. In group 4, H+ secretion in the collecting duct, as assessed by analyzing the relationship between urine-minus-blood PCO2 and urinary bicarbonate concentration in maximally alkaline urine, was not modified during CaCl2 infusion [delta(Ca)P, 0.79 mM]. We conclude that increase in plasma calcium concentration inhibits proximal NaCl and water reabsorption, whereas it stimulates the bicarbonate transport relative to that of chloride, leading to an enhanced proximal and renal bicarbonate-to-chloride reabsorptive ratio that could generate metabolic alkalosis; and decreases urinary bicarbonate excretion by also lowering the bicarbonate filtered load.

Absorption↗

PubMed1986

Effects of parathyroid hormone on urinary acidification.

Recollection micropuncture experiments were carried out in plasma-replete euvolemic thyroparathyroidectomized rats to examine the effects of a purified bovine parathyroid hormone (PTH) infusion on urinary acidification. After a 60-min equilibration period, PTH administration had the following effects: reabsorption in the proximal convoluted tubule was inhibited 13% for total CO2, 31% for chloride, and 28% for water; early distal delivery, however, remained unchanged for bicarbonate, chloride, and water principally as a result of stimulation of bicarbonate and chloride absorption in Henle's loop; the urinary bicarbonate and chloride excretion rates did not vary significantly, but the urinary pH decreased from 6.78 +/- 0.11 to 6.39 +/- 0.07 and titratable acid and ammonium excretion increased from 63 +/- 18 to 405 +/- 45 and from 422 +/- 30 to 647 +/- 44 nmol X min-1 X g kidney wt-1, respectively. In another group of rats, the bicarbonate urinary excretion rate increased more than twofold during the first 60 min of PTH infusion and then returned to control levels as was observed in the other groups; the transient increase in bicarbonaturia was attributable to a PTH-induced transient augmentation in glomerular filtration rate and bicarbonate filtered load. Finally, no change was noted in micropuncture or whole-kidney data in time-control rats. We conclude that PTH only transiently enhances the bicarbonate filtered load and urinary excretion rate during the first 60 min of administration secondary to an early hemodynamic action but that the steady effect is to stimulate urinary acidification and net acid excretion, which could generate metabolic alkalosis; and that the inhibition of the proximal bicarbonate and chloride reabsorption induced by PTH is counterbalanced by stimulation of reabsorption in Henle's loop.

Absorption↗

PubMed1986

Pseudohypoaldosteronism type II: proximal renal tubular acidosis and dDAVP-sensitive renal hyperkalemia.

The mechanisms of metabolic acidosis and hyperkalemia were investigated in a patient with chronic mineralocorticoid-resistant renal hyperkalemia (5.3-6.9 mmol/l), metabolic acidosis (arterial blood pH 7.27, total CO2 17 mmol/l), arterial hypertension, undetectable plasma renin activity (less than 0.10 ng/ml/h), high plasma aldosterone level (32-100 ng/dl), and normal glomerular filtration rate (131 ml/min/1.73 m2). During the hyperkalemic period, urine was highly acidic (pH 4.6-5.0), urinary NH4 excretion (10-13 microEq/min) and urinary net acid excretion (19-24 microEq/min) were not supernormal as expected from a chronic acid load. During NaHCO3 infusion, the maximal tubular HCO3 reabsorption was markedly diminished (19.8 mmol/l glomerular filtrate), and the fractional excretion of HCO3 (FE HCO3) when plasma HCO3 was normalized was 20%. Urine minus blood PCO2 increased normally during NaHCO3 infusion (31 mm Hg), and the urinary pH remained maximally low (less than 5.3) when the buffer urinary excretion sharply increased after NH4Cl load. When serum K was returned toward normal limits, metabolic acidosis disappeared, urinary NH4 excretion rose normally after short NH4Cl loading while the urinary pH remained maximally low (4.9-5.2), the maximal tubular HCO3 reabsorption returned to normal values (24.8 mmol/l glomerular filtrate), and FE HCO3 at normal plasma HCO3 was 1%. Nasal insufflation of 1-desamino-8-D-Arginine Vasopressin (dDAVP) resulted in an acute normalization of the renal handling of K and in an increase in net urinary acid excretion. We conclude that: the effect of dDAVP on renal handling of K may be explained by the reversal of the distal chloride shunt and/or an increase in luminal membrane conductance to K; the distal acidification seems to be normal which in the event of distal chloride shunt impairing distal hydrogen secretion might be explained by the presence of systemic acidosis which is a potent stimulus of hydrogen secretion, and metabolic acidosis in the steady state was accounted for by the diminution of bicarbonate reabsorption and ammonia production in the proximal tubule secondary to chronic hyperkalemia.

Acid-Base Equilibrium↗

PubMed1986

Renal hemodynamic effects of tertatolol in essential hypertension.

Tertatolol, a new beta-blocker, and propranolol, considered a reference beta-blocker, were given orally (5 and 160 mg slow release, respectively) for 15 days to two groups of patients with essential hypertension in order to compare their effects on renal hemodynamics. Systolic and diastolic blood pressure, heart rate, and erect plasma renin activity fell significantly in both groups while prostaglandin E2 urinary excretion was unchanged. Tertatolol administration produced increases in glomerular filtration rate, as shown by inulin clearance (+8.9%; p = 0.038) and renal plasma flow, as shown by paraaminohippurate clearance (+13.0%; p = 0.007). In contrast, propranolol administration resulted in a slight decrease in glomerular filtration rate (-2.8%; not significant) and a fall in renal plasma flow (-13.4%; p less than 0.001). Comparison between both treatments showed that glomerular filtration rate and renal plasma flow were higher in the patients treated with tertatolol than in those treated with propranolol whereas filtration fraction was lower, which suggests that tertatolol causes a vasodilation of the glomerular afferent arteriole. These results demonstrate that in contrast to propranolol (160 mg), and despite both drugs exhibiting a comparable antihypertensive activity, tertatolol (5 mg) does not alter but even improves renal perfusion in hypertensive patients.

Adrenergic beta-Antagonists↗

PubMed1985

Parathyroid hormone contributes to volume expansion-induced inhibition of proximal reabsorption.

Volume expansion inhibits the proximal reabsorption of water, bicarbonate, and chloride. The present work tested a hypothetical role of parathyroid hormone (PTH) in the expansion effect. We studied 19 Sprague-Dawley rats during a plasma-replete euvolemic state and following 10% body wt colloid-free expansion. In group I, six intact rats, volume expansion decreased plasma ionized calcium concentration ([Ca2+]P) from 2.28 +/- 0.06 to 2.11 +/- 0.04 meq/liter and increased nephrogenous cAMP (NcAMP) from 29 +/- 5 to 66 +/- 10 pmol X min-1 X g kidney wt-1. In group II, six acutely thyroparathyroidectomized (TPTX) rats, [Ca2+]P also fell from 2.18 +/- 0.08 to 1.80 +/- 0.08 meq/liter but NcAMP did not rise significantly (9 +/- 3 vs. 17 +/- 5 pmol X min-1 X g kidney wt-1). These data strongly suggest that stimulation of PTH activity occurred during expansion in intact animals. In group III, seven TPTX rats, volume expansion inhibited proximal reabsorption of total CO2 by 11%, of chloride by 24%, and of water by 19%. Volume expansion-induced reduction in bicarbonate, chloride, and water reabsorption was smaller in TPTX than in intact rats previously studied. We conclude that volume expansion inhibits proximal reabsorption in part by decreasing the active transcellular NaHCO3 and NaCl transport secondary to stimulation of PTH activity.

Absorption↗

PubMed1985

[Type II pseudohypoaldosteronism: proximal tubular acidosis and distal tubular hyperkalemia corrected by DDAVP].

The mechanisms of metabolic acidosis and hyperkalemia were investigated in a patient with chronic mineralocorticoid-resistant renal hyperkalemia (5.3 to 6.8 mM), metabolic acidosis (arterial blood pH 7.27, total CO2 17 mM), arterial hypertension, undetectable plasma renin activity (less than 0.10 ng/ml/hr), high plasma aldosterone (32 to 100 ng/dl), normal GFR (131 +/- 2.5 ml/min/1.73 m2). During hyperkalemic period, urine was highly acidic (pH 4.6 to 5.0), urinary NH4 excretion (13 mumoles/min) and urinary net acid excretion (24 mumoles/min) were not supernormal as expected from a chronic acid load. During NaHCO3 infusion, maximal tubular HCO3 reabsorption (Tm HCO3) was markedly diminished (19 mmoles/liter GF), fractional excretion of HCO3 (FE HCO3) when plasma HCO3 was normalized, was 20%. Urine-minus-blood PCO2 increased normally (31 mmHg) during NaHCO3 infusion, and urinary pH remained maximally low (less than 5.3) when buffer urinary excretion sharply increased after NH4Cl load. When serum K was returned toward normal limits, metabolic acidosis disappeared, urinary NH4 excretion rose normally after short NH4Cl loading while urinary pH remained maximally low (4.9 to 5.2), Tm HCO3 returned to normal value (24.8 mmoles/liter GF), and FE HCO3 became nil. The renal handling of K was improved with acute NaHCO3 loading and normalized after DDAVP nasal insufflation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗

PubMed1984

Volume expansion modulates NaHCO3 and NaCl transport in the proximal tubule and Henle's loop.

The effects of extracellular fluid volume expansion on kidney reabsorption of bicarbonate, chloride, and water were examined in Sprague-Dawley rats by paired micropuncture experiments in which tubular fluid was collected from early distal and end-proximal sites. In group I, rats were studied during a plasma-replete euvolemic state and after 10% body wt colloid-free volume expansion. The filtered loads were similar in euvolemia and expansion; expansion increased end-proximal total CO2 concentration ([tCO2] EP) from 13.0 +/- 0.8 to 18.4 +/- 0.7 mM and inhibited the tCO2 fractional reabsorption 26% in the proximal convoluted tubule and 15% in Henle's loop. Early distal tCO2 delivery therefore increased from 61 +/- 7 to 140 +/- 17 pmol X min-1 X g kidney wt-1. A more pronounced inhibition of fractional reabsorption of chloride (45%) and water (35%) occurred in the proximal convoluted tubule during expansion. In group II, rats were studied during 5% body wt 70 g/liter albumin-containing expansion and after 10% body wt colloid-free expansion. Compared with euvolemia of group I, albumin expansion decreased proximal fractional reabsorption of tCO2 13%, chloride 19%, and water 14% without change in filtered loads, and [tCO2]EP rose to 17.2 +/- 0.7 mM. A 10 g/liter decrease in plasma protein concentration during colloid-free expansion was associated, compared with albumin expansion, with inhibition of proximal fractional reabsorption of tCO2 by 4%, chloride by 18%, and water by 9% without further altering [tCO2]EP. We conclude that 1) expansion specifically inhibits bicarbonate reabsorption in the proximal convoluted tubule and in Henle's loop independent of change in filtered load or in peritubular protein concentration, probably by enhancing bicarbonate backdiffusion and reducing proton secretion; 2) expansion-induced decrease in peritubular protein concentration contributes to the proximal expansion effect probably by specifically inhibiting transcellular sodium chloride reabsorption.

Animals↗

PubMed1983

Na:H exchange and the primary H pump in the proximal tubule.

Cell pH (pHi) transients were monitored at 5-min intervals with the weak acid 5,5-[14C]dimethyloxazolidine-2,4-dione and membrane potentials were estimated from the distribution of [3H]triphenylmethylphosphonium ion in separated proximal tubules (SPT) or rabbit kidney. SPT suspensions were gassed at 37 degrees C first with 5% CO2 and then with 15% CO2. Under normal conditions, pHi rapidly fell during initial 15% CO2 acid loading and then recovered within 20 min. In the presence of 10(-3) M ouabain, which eliminated Na:H exchange as a driving force for H+ secretion, initial cell acidification was still followed by cell pH recovery, which demonstrated a sodium gradient-independent H+ extruding mechanism. In the presence of 10(-3) M ouabain plus 10(-4) M potassium cyanide, there was no pHi recovery following initial cell acidification but, on the contrary, further progressive cell acidification occurred, which is compatible with passive diffusion only of HCO-3 out of the cell. From the cyanide experiments, an apparent permeability coefficient for HCO-3 of the basolateral cell membrane was calculated; this latter result allowed the calculation of rates of passive HCO-3 diffusion and of active H+ extrusion under normal conditions and in the presence of 10(-3) M ouabain. We conclude that in the proximal tubule 1) there is a primary H+ pump additional to Na:H exchange; and 2) this primary H+ pump is responsible for about 25% of active H+ extrusion following acute CO2 cellular acid loading.

Animals↗

PubMed1980

Hydrogen transport in rabbit kidney proximal tubules--Na:H exchange.

In order to examine the cellular mechanisms of H transfer, we studied the [14C]DMO-derived cell pH in rabbit separated renal proximal tubules. Under normal conditions, cell pH (7.508 +/- 0.008, SE) was found to be more alkaline than medium pH (7.404 +/- 0.009, SE). The [14C]DMO-derived cell pH was not affected either by 10(-2) M unlabeled DMO or 10(-3) M probenecid. Removal of external sodium resulted in cell acidification. Addition or 10(-3) M ouabain to the medium dissipated the transmembrane sodium gradient [Na]o/[Na]i and lowered cell pH. However, the DMO-derived cell pH observed in the presence of ouabain was higher than the calculated cell pH, assuming passive distribution of H ions across the cell membrane. In the presence of ouabain, reducing [Na]o/[Na]i led to cell acidification, and augmenting [Na]o/[Na]i caused cell alkalinization. These results indicate that in the proximal tubule: 1) the H transfer from cell to lumen is active, whereas the HCO3 transfer across the basal membrane may be passive; 2) there is evidence for a Na:H exchange via a countertransport mechanism; and 3) Na:H exchange may not be the only mechanism responsible for active H transfer.

Animals↗

PubMed1979

Regulation of cell volume in separated renal tubules incubated in hypotonic medium.

The regulation of cell volume was studied in separated renal tubules (SRT) whose basement membrane had been removed by collagenase. Regulation occurred when SRT were immersed in a hypotonic medium, the increase in cellular water content being half that expected in the absence of regulation. Regulation was immediate, with no initial swelling, and was accompanied by a loss of NaCl, with no change in cellular K. This regulation was eliminated by 10(-3) M ouabain. We conclude that: 1) Cell volume regulation which occurs in a hypotonic medium is due to an immediate loss of NaCl. 2) Loss of NaCl might be due to blocking of the net passive NaCl entry into the cells resulting from the drop in the transmembrane NaCl electrochemical gradient. The high membrane sodium permeability, probably located on the luminal side of the tubular cells, might explain why regulation was instantaneous. 3) Elimination of volume regulation by ouabain suggests there is no need to assume that a ouabain-insensitive pump regulates cell volume.

Animals↗

PubMed1974