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Biomedical subjects

H Favre

Publications and source records attributed to H Favre.

At least 19 recordsLinked to original sources
PubMed1996

Preoperative inhibition of angiotensin-converting enzyme improves systemic and renal haemodynamic changes during aortic abdominal surgery.

We studied 22 patients undergoing aortic surgery, allocated randomly to receive, before induction of anaesthesia, a single i.v. dose of enalapril 50 micrograms kg-1 or saline. During infrarenal aortic cross-clamping, we observed similar reductions in oxygen uptake in the two groups, despite greater systemic oxygen delivery in enalapril-treated patients; angiotensin-converting enzyme inhibition prevented the reduction in cardiac output and attenuated the decrease in glomerular filtration. Changes in glomerular filtration secondary to aortic clamping were related positively to changes in renal plasma flow (r = 0.83 (saline group) and r = 0.65 (enalapril group)). Creatinine clearance on the first day after operation was significantly higher in the enalapril compared with the saline group. We conclude that enalapril pretreatment is effective in improving systemic oxygen delivery, renal plasma flow and glomerular filtration during aortic abdominal surgery.

Aged↗
PubMed1996

Protein kinase C-dependent phosphorylation of Na(+)-K(+)-ATPase alpha-subunit in rat kidney cortical tubules.

We have previously shown that, in oxygenated rat kidney proximal convoluted tubules (PCT), activation of protein kinase C (PKC) by phorbol 12,13-dibutyrate (PDBu) directly stimulates Na(+)-K(+)-adenosinetriphosphatase (ATPase) activity. PKC modulation of Na(+)-K(+)-ATPase activity by phosphorylation of its alpha-subunit was the postulated mechanism. The present study was therefore designed to investigate the relationship between PKC-mediated phosphorylation of the catalytic alpha-subunit and the cation transport activity of the Na(+)-K(+)-ATPase. In a suspension of rat kidney cortical tubules, activation of PKC by 10(-7) M PDBu increased the level of phosphorylation of the Na(+)-K(+)-ATPase alpha-subunit and stimulated the ouabain-sensitive 86Rb uptake by 47 and 42%, respectively. Time and dose dependence of the PDBu-induced increase in Na(+)-K(+)-ATPase activity and phosphorylation was strongly linearly correlated. The effects of PDBu on phosphorylation and activity of Na(+)-K(+)-ATPase were prevented by GF-109203X, a specific PKC inhibitor, whereas H-89, a specific PKA inhibitor, was ineffective. These results demonstrate that PKC activation induces phosphorylation of the catalytic alpha-subunit of Na(+)-K(+)-ATPase, which may participate in the stimulation of its cation transport activity in the rat PCT.

Animals↗
PubMed1996

Complement depletion during haemofiltration with polyacrilonitrile membranes.

BACKGROUND: Polyacrylonitrile (PAN, AN69) dialysis membranes have been shown to improve the outcome of critically ill patients. Factor D is an essential enzyme of the alternative pathway of complement and is increased during renal failure. On the other hand the contact of blood with biomaterials activates the complement cascade through the alternative pathway. PAN filters adsorb factor D which looses its enzymatic activity whilst bound to the membrane [1]; the complement alternative pathway function of serum exposed to PAN filters is greatly diminished and restored after addition of purified factor D [1]. The aim of our study was to measure the time course of factor D adsorption and its blood concentration during CVVH in critically ill patients with acute renal failure. METHODS: We studied seven critically ill patients with ARF before, during and after continuous veno-venous haemofiltration (CVVH) with AN69. RESULTS: There was a rapid decrease of factor D levels to 62(+/-6%) of the pre-CVVH value during the first 2 h, which continued to 51(+/-7.3%) after 12 h; at 24 h there was a slight rise to 62 +/- 12%. Sequential use of Polyacrylonitrile (AN69) filters lowered factor D levels below the normal plasma concentration in three patients, thus producing a state of factor D depletion. CONCLUSION: The significant reduction of factor D levels during CVVH with PAN filters suggests that frequent changes of PAN filters may reduce alternative pathway function by lowering factor D levels. CVVH (as opposed to intermittent dialysis) with PAN membranes may further improve the outcome of critically ill patients.

Acrylic Resins↗
PubMed1995

Effect of insulin on Na+,K(+)-ATPase in rat collecting duct.

1. The collecting duct is involved in the whole antinatriuretic effect of insulin, as indicated in vitro by the stimulatory effect of the hormone on ouabain-sensitive 86Rb+ uptake. Since Na+,K(+)-ATPase drives Na+ reabsorption, the contribution of the Na+ pump to the effect of insulin was investigated in rat isolated cortical and outer medullary collecting duct. 2. Insulin enhanced ouabain-sensitive 86Rb+ uptake in the absence, as well as in the presence, of either 5 x 10(-4) M amiloride or 10(-3) M hydrochlorothiazide (HCT). Maximal ouabain-sensitive 86Rb+ uptake, measured in Na(+)-loaded tubules, was also enhanced by insulin. The insulin effect persisted both in the absence of external Na+, when the Na+,K(+)-ATPase operates in a Rb(+)-Rb+ exchange mode, and in tubules depolarized by a high external concentration (20 mM) of Rb+ or by addition of 3 mM Ba2+. 3. Insulin treatment did not alter the intracellular Na and K concentrations, the specific binding of [3H]ouabain measured in intact tubules, or the hydrolytic activity of Na+,K(+)-ATPase measured after permeabilization of the tubule cells. 4. In conclusion, in the rat collecting duct, insulin increased Na+,K(+)-ATPase-mediated cation transport independently of Na+ availability, membrane potential and recruitment of pump units. The effect of insulin was lost after cell permeabilization, suggesting the presence of a cytosolic factor which controls the turnover of Na+,K(+)-ATPase.

Adenosine Triphosphate↗
PubMed1995

[Acute kidney failure in tubular necrosis].

Tubular necrosis is the most frequent hospital-acquired cause of acute renal failure from renal origin. The two main factors leading to tubular necrosis are hemodynamic perturbations and use of nephrotoxic agents. There is recently a growing number of reports on tubular necrosis associated with a non traumatic rhabdomyolysis. In 60-70% of the cases, more than one contributing factor can be identified. In the majority of the patients who developed a transient postoperative acute renal failure, co-morbid factors such as diabetes, hypertension or major cardiovascular problems, are present. Acute renal failure increases the mortality by factors from 2-7. Therefore prevention and (or) early correction of the factors leading to tubular necrosis are of great importance.

Acute Kidney Injury↗
PubMed1995

Presence of two isoforms of Na, K-ATPase with different pharmacological and immunological properties in the rat kidney.

Previous studies have demonstrated the presence of two populations of Na,K-ATPase with distinct kinetic, pharmacological and immunological characteristics along the rabbit nephron, indicating that the proximal segments of the nephron express exclusively the alpha 1 isoform of the catalytic subunit, whereas the collecting duct expresses an alpha 3-like isoform. Because pharmacological studies have shown the existence of two populations of Na,K-ATPase with different sensitivities to ouabain in the rat cortical collecting duct, which may result from the presence in the same nephron segment of the two isoforms demonstrated in the different segments of the rabbit nephron, the present study was undertaken to characterize the properties of Na,K-ATPase along the rat nephron. Results indicate that each segment of the rat nephron contains two subpopulations of Na,K-ATPase: a component highly sensitive to ouabain (IC50 approximately 5.10(-6) M) which is recognized by an anti-alpha 3 antibody and another moiety of lower affinity for ouabain (IC50 approximately 5.10(-4) M) which is recognized by an anti-alpha 1 antibody. Whether these two subpopulations correspond to different isoforms of the alpha subunit of Na,K-ATPase (alpha 1 and alpha 3-like) remains to be determined.

Amino Acid Sequence↗
PubMed1995

Insulin unresponsiveness of tubular monovalent cation transport during fructose-induced hypertension in rats.

1. Hyperinsulinaemia is considered to be a pathogenic factor for human and experimental hypertension. Thus, the contribution of the known insulin-stimulated tubular sodium reabsorption to this aetiological process has to be discussed. 2. Rats fed a fructose-enriched diet develop hyperinsulinaemia and hypertension, providing a model for studying the regulation of the tubular sodium handling and its possible relationship to hypertension. For this purpose, the sodium transport capacity of isolated nephron segments from control rats and from rats fed a fructose-enriched diet was investigated by measurement of ouabain-sensitive 86Rb uptake and of the hydrolytic activity of Na,K-ATPase. The number and affinity of insulin receptors were estimated from the specific [125I]insulin binding. 3. In rats fed a fructose-enriched diet, mild hypertension developed during the 14-day fructose diet. There were no differences, along the nephron, in basal 86Rb uptakes and ATPase activities between control rats and fructose-induced hypertensive rats. In control rats, insulin stimulated 86Rb uptake in the proximal convoluted tubule and cortical collecting duct, but exhibited an inhibitory action in the medullary thick ascending limb. In contrast, in fructose-induced hypertensive rats, 86Rb influx remained unresponsive to insulin concentrations ranging from 10(-11) to 10(-7) mol/l in the proximal convoluted tubule and cortical collecting duct. In the medullary thick ascending limb, the threshold of inhibition was displaced from 10(-11) mol/l up to 10(-7) mol/l. Insulin binding to the proximal convoluted tubule, medullary thick ascending limb and collecting duct were similar in control rats and in rats fed a fructose-enriched diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Protein kinase C-dependent stimulation of Na(+)-K(+)-ATP epsilon in rat proximal convoluted tubules.

In rat proximal convoluted tubule (PCT), activation of protein kinase C (PKC) by phorbol 12,13-dibutyrate (PDBu) was previously reported to inhibit Na(+)-K(+)-ATPase, a paradoxical finding in view of the known stimulatory effect of PKC on Na+ reabsorption. Because this inhibition occurs via phospholipase A2 activation, a pathway stimulated by hypoxia, we evaluated the influence of oxygen supply on PKC action on Na(+)-K(+)-ATPase. Results confirmed that PDBu inhibited PCT Na(+)-K(+)-ATPase activity under usual conditions. In contrast, when oxygen supply was increased, PDBu had no effect on Na(+)-K(+)-ATPase hydrolytic activity, but it dose-dependently stimulated ouabain-sensitive 86Rb+ uptake. This latter effect, which was abolished by PKC inhibitors, resulted from an increment of the Na+ sensitivity of Na(+)-K(+)-ATPase. Thus, in oxygenated rat PCTs, activation of PKC primarily stimulated Na(+)-K(+)-ATPase. This likely contributes to increase solute reabsorption. Inhibition of Na(+)-K(+)-ATPase was observed only under hypoxic conditions. It may represent an adaptation to protect PCTs against deleterious effects of hypoxia.

Animals↗
PubMed1994

Anticoagulation in patients treated by continuous venovenous hemofiltration: a retrospective study.

The most adequate anticoagulation regimen during extracorporeal renal replacement therapy can be difficult to define. Two hundred fifty-five critically ill patients with a mean age (+/- SD) of 58.2 +/- 16.3 years were treated by continuous venovenous hemofiltration (CVVH) between 1986 and 1992 in our intensive care units. Blood was circulated through hemofilters, either polyacrylonitrile (AN 69; Hospal, Lyon, France) or polyamide (FH 66; Gambro, Lund, Sweden), using a roller pump and an air safety system. The patients were classified into three subgroups according to the amount of heparin needed to achieve an adequate anticoagulation (ie, prevention of extracorporeal circuit clotting without inducing a patient's bleeding tendency): group 1, 37 patients who received no heparin (14.5%); group 2, 189 patients who received 100 to 700 IU/hr of heparin (74.1%); and group 3: 29 patients who received more than 700 IU/hr of heparin (11.4%). We analyzed the filter survival, the routine coagulation parameters, and the evolution of the patients for each group. Median duration of treatment was 144 hours (range, 4 to 1,152 hours). There were no differences in requirement of heparin among the two types of membrane: AN 69 (mean +/- SD), 393 +/- 106 IU/hr v FH 66, 374 +/- 35.3 IU/hr (range, 0 to 2,000 IU/hr). There were no relationships between the amount of heparin the patients received and the mean survival of the filters (group 1, 22.1 +/- 14.8 hr; group 2, 24.7 +/- 13.2 hr; group 3, 23 +/- 9.6 hr).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Insulin enhances sodium sensitivity of Na-K-ATPase in isolated rat proximal convoluted tubule.

Insulin has been shown to stimulate the rate of ouabain-sensitive 86Rb influx in the isolated rat proximal convoluted tubule (PCT). To study the mechanism of this activation of Na-K-adenosinetriphosphatase (Na-K-ATPase), we determined the actions of insulin on 1) the maximal activity (Vmax) of Na-K-ATPase hydrolytic activity; 2) the maximal rate of ouabain-sensitive 86Rb influx (after intracellular Na loading); 3) the rate of ouabain-sensitive 86Rb influx under conditions where intracellular Na concentration is rate limiting, either in the presence or in the absence of 5 x 10(-4) M amiloride and/or low extracellular Na concentration (3 mM); and 4) the Na sensitivity of the Na-K-ATPase hydrolytic activity. The maximal rates of Na-K-ATPase hydrolytic activity and of ouabain-sensitive 86Rb uptake were unchanged by insulin. In contrast, we confirmed that insulin enhanced 86Rb uptake (in peq.mm-1.min-1) in the absence of inhibitor of the Na/H exchanger [18.2 +/- 1.7 to 24.1 +/- 1.3 (SE), P < 0.03] and, in addition, demonstrated a similar stimulation in the presence of either 5 x 10(-4) M amiloride (7.2 +/- 0.6 to 10.7 +/- 0.9, P < 0.01), 3 mM extracellular Na (4.1 +/- 0.4 to 5.6 +/- 0.2, P < 0.05), and both amiloride and 3 mM extracellular Na (2.1 +/- 0.7 to 4.5 +/- 0.4, P < 0.03). Finally, insulin increased the sensitivity of Na-K-ATPase to Na as the apparent dissociation constant decreased from 46.5 +/- 5.3 to 27.6 +/- 3.0 mM (P < 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed1993

Fenoldopam improves renal hemodynamics impaired by positive end-expiratory pressure.

BACKGROUND: Mechanical ventilation with positive end-expiratory pressure (PEEP) can impair renal hemodynamics. Fenoldopam, a dopamine receptor agonist, has been shown, in animal experiments, to improve renal perfusion. The purpose of the current study was to examine the effects of this agent on altered renal hemodynamics secondary to positive pressure ventilation. METHODS: Twelve patients requiring mechanical ventilation of their lungs and PEEP for the treatment of hypoxemia after multiple trauma or visceral surgery were studied. Hemodynamic variables, renal vascular resistance, urine flow, creatinine, inulin and PAH clearance, and excretion of sodium and potassium (NaE and KE) were measured before and after introduction of a level of PEEP high enough to decrease urine flow rate by 25% or more, and after administration of intravenous fenoldopam. RESULTS: No hemodynamic effect resulted from 0.1 microgram.kg-1.min-1, but 0.2 micrograms.kg-1.min-1 fenoldopam decreased both diastolic and mean arterial blood pressure from 66 +/- 37 (mean +/- SEM) to 57 +/- 21 mmHg, and from 83 +/- 3 to 74 +/- 4 mmHg, respectively. Renal vascular resistance was reduced from 54 +/- 12 to 19 +/- 5 dynes.s.cm-5 at 0.2 micrograms.kg-1.min-1. Fenoldopam produced a dose-related increase in renal blood flow and PAH clearance. With 0.2 micrograms.kg-1.min-1 fenoldopam, urine flow increased from 81 +/- 25 to 116 +/- 29 ml/h, NaE from 28 +/- 7 to 85 +/- 70 microM/min, and KE from 65 +/- 12 to 109 +/- 16 microM/min. CONCLUSIONS: The results of the current study indicate that intravenous fenoldopam at a dose of 0.2 micrograms.kg-1.min-1 improves renal hemodynamics and increases Na and K excretion in patients requiring mechanical ventilation of their lungs and PEEP. These effects are probably caused by an increased kidney perfusion secondary to renal artery vasodilation.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1993

Natriuretic and vasoactive hormones and glomerular hyperfiltration in hyperglycaemic type 2 diabetic patients: effect of insulin treatment.

Evidence that an increase in plasma atrial natriuretic peptide (ANP) concentrations mediates, at least in part, glomerular hyperfiltration in diabetic rats prompted us to study the relationship between ANP and renal haemodynamics in hyperfiltering type 2 diabetic patients in association with other hormones implicated in the control of glomerular filtration rate (GFR) (catecholamines, vasopressin, renin) and in sodium tubular transport (aldosterone, ouabain-displacing factor, ODF). Since hyperglycaemia is also associated to hyperfiltration, diabetic patients who presented with secondary drug failure were studied both in hyperglycaemic and in normoglycaemic condition. For this purpose, 11 normotensive non-macroproteinuric hyperfiltering patients with type 2 diabetes were treated with an 8-day continuous insulin infusion (days 0-7). Dehydration was prevented or corrected and natriuresis was on day 0 above 100 mmol/day. The following parameters were determined on days 0 and 7: GFR and renal plasma flow (RPF) by 99mTc-DTPA and 131I-hippuran clearances; the extracellular volume, assimilated to the DTPA diffusion volume; urinary ODF by receptor-binding assay and urinary as well as plasma catecholamines by HPLC after extraction on alumin. Plasma ANP and antidiuretic hormone (ADH) were measured by radioimmunoassay after extraction on phenyl-silylsilica (ANP) and with ether (ADH). Unextracted plasma was used for radioimmunological measurement of plasma renin activity and aldosterone. When correcting hyperglycaemia to normoglycaemia GFR decreased from high to normal mean value (138 +/- 27 and 115 +/- 6 ml/min, p < 0.001), RPF followed the same trend, and the DTPA diffusion volume did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗