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Biomedical subjects

C Amiel

Publications and source records attributed to C Amiel.

At least 127 records · Page 7Linked to original sources

Na and nonelectrolyte entry into inner ear fluids of the rat.

Kinetics of hydrophilic solute entry into endolymph (EL), perilymph (PL), and cerebrospinal fluid (CSF) were studied after intravenous administration (sodium, urea, glycerol, mannitol, sucrose) and cerebral lateral ventricle injection (urea, sucrose) of tracers in anesthetized rats. Samples of cochlear EL, PL of scala vestibuli (PLV), PL of scala tympani (PLT), and cisternal CSF were obtained. The data showed slow entry of tracers in PLV, PLT, and CSF as follows: Na greater than urea greater than mannitol approximately sucrose; slower entry of mannitol and sucrose in PLT and CSF than in PLV; 1 h delayed peak of radioactivity in PLV compared with the immediate peaks in PLT and CSF after CSF injection, and the value of PLV peak was 13% that in CSF; extremely slow entry of nonelectrolytes in EL. These results indicate that PLV originates mainly from plasma across a blood-perilymph barrier that restricts the entry of small hydrophilic solutes. The blood-perilymph barrier is most likely composed of an endothelial barrier associated with an epithelial secretion. The latter could be located at the vasculo-epithelial zone of the spiral limbus.

Animals↗

Facilitated transfer of glucose from blood into perilymph in the rat cochlea.

The transport of glucose into cochlear endolymph, perilymph of scala vestibuli and perilymph of scala tympani, and cerebrospinal fluid (CSF) was studied after intravenous administration of tracers of D-glucose, L-glucose, and 3-O-methyl-D-glucose in anesthetized rats. The data showed that D-glucose concentrations in perilymph of scala vestibuli, perilymph of scala tympani, and CSF were approximately 50%, and in endolymph less than 10%, that in plasma; D-glucose concentration in perilymph of scala vestibuli, perilymph of scala tympani, and CSF increased as a linear function of that in plasma; D-glucose entry into perilymph of scala vestibuli, perilymph of scala tympani, and CSF was more rapid than that of L-glucose; after infusion of 3-O-methyl-D-glucose, but not after that of mannitol, both the D-glucose concentration ratio of perilymph over plasma and D-glucose transfer into perilymph were lowered. These results indicate that D-glucose enters into perilymph of scala vestibuli by a facilitated transport, possibly located at the blood-perilymph barrier.

3-O-Methylglucose↗

HSV1 strain sensitivity in experimental rabbit keratitis: evolution under repeated topical IDU administrations.

The effects of repeated topical idoxuridine (IDU) administration of HSV1 strain sensitivity were investigated during 6 serial passages (P1 to P6) in the rabbit. By comparison to placebo treated rabbits, a delay in ulcer cicatrization appeared at P2 and clinical resistance was completed at P3. Clinical cross resistance to acyclovir (ACV) was also tested and demonstrated at P7. In vitro, a plaque reduction test on Vero cells using directly the tear film HSV populations allowed the prediction of the resistance by an early rise in the effective dose 90% (ED 90) value anticipating that in ED 50%. An ED 50 determination by dye-uptake assay on P6 HSV isolate demonstrated a cross resistance to viral thymidine kinase (TK) dependent drugs without any change in Ara-A and PFA sensitivity, according to a 23% TK activity at P6. At the last passage the HSV drug resistant population had an unrestricted corneal pathogenicity. A return to IDU and ACV in vitro sensitivity was demonstrated in group control animals at P2 but not at P4 or P6.

Acyclovir↗

Somatostatin and alpha 2-adrenergic agonists selectively inhibit vasopressin-induced cyclic AMP accumulation in MDCK cells.

The effect of somatostatin and alpha 2-adrenergic agonists on cyclic AMP accumulation was examined in MDCK cells, grown in defined medium. These hormones inhibited vasopressin-induced cyclic AMP formation, without affecting either the basal or the glucagon- and prostaglandin E2-stimulated level. Pretreating the cells with pertussis toxin, or incubating them with MnCl2 at a low concentration reversed the effect of somatostatin and alpha 2-agonists. These results suggest that somatostatin and norepinephrine could selectively modulate the renal effect of vasopressin, via the inhibitory regulatory subunit (Ni) of adenylate cyclase.

Adenylate Cyclase Toxin↗

Stimulation by glucagon and PTH of Ca and Mg reabsorption in the superficial distal tubule of the rat kidney.

The effects of glucagon and PTH on electrolyte reabsorption in the distal tubule were investigated in rats deprived of vasopressin, calcitonin, PTH, and glucagon. Micropunctures of distal tubule, at a late and an early site of a same nephron, have been performed in 23 rats, nine control, seven infused with glucagon (5 ng X min-1 X 100 g-1 b.w.) and seven with PTH (5 mU X min-1 X 100 g-1 b.w.). The Ca and Mg reabsorptive capacity of the distal segment was increased by glucagon and by PTH. Moreover, fractional Na and Cl reabsorption was significantly higher than in control during PTH administration. A K secretion appeared during the administration of both hormones. No phosphate net transport was observed in any group. Finally, the data presented here, together with those previously reported, indicate that the increase of Ca and Mg renal reabsorption observed with glucagon and PTH results from an effect located in both Henle's loop, where the bulk of Ca and Mg is reabsorbed, and the distal tubule.

Absorption↗

Decreased calcium and magnesium urinary excretion during prostaglandin synthesis inhibition in the rat.

The effect of endogenous renal prostaglandins on calcium and magnesium reabsorption was investigated. Renal tubular handling of calcium and magnesium was studied by clearance methods in anesthetized Sprague-Dawley and Brattleboro rats, either intact or thyroparathyroidectomized (ATPTX), before and during prostaglandin synthesis inhibition by meclofenamate, indomethacin, or piroxicam infusion. These three inhibitors had similar effects on calcium and magnesium excretion: A significant decrease in absolute and fractional excretions of both cations was observed in intact Sprague-Dawley rats, and in ATPTX rats of both strains, but not in intact Brattleboro rats. These results suggest an inhibitory effect of prostaglandins on vasopressin-, glucagon-, but not PTH-mediated calcium and magnesium reabsorption. This effect is likely to occur in the thick ascending limb of Henle, which is both a target site for these polypeptidic hormones, and a segment where the bulk of calcium and magnesium is reabsorbed.

Animals↗

Relative contribution of intrinsic lung dysfunction and hypoventilation to hypoxemia during hemodialysis.

Two mechanisms have been proposed to explain hemodialysis (HD)-induced hypoxemia: reversible lung damage due to intrapulmonary leukostasis as a consequence of the contact of blood with the dialyzer membrane, or alveolar hypoventilation due to the loss of carbon dioxide through the dialyzer. To assess the role of these factors, seven chronically uremic patients were studied before and during 4-hr HD sessions using a cuprophane membrane and either acetate (AHD) or bicarbonate (BHD) dialysate. In AHD only we observed, by comparison with predialysis values, a significant hypoxemia, and a decrease of alveolar ventilation (VA), lung carbon dioxide output, and respiratory exchange ratio. In both the AHD hypoxemic group and BHD nonhypoxemic group, there was a similar decrease in lung carbon dioxide diffusing capacity (DLCO) and of white blood cells (WBC), and a positive correlation between arterial oxygen pressure and VA without modification of alveolo arterial PO2 difference, an argument against the existence of ventilation-perfusion or ventilation-diffusion mismatching. We conclude that, although WBC sequestration induced a lung damage evidenced by DLCO impairment, the key factor of hypoxemia observed in AHD was the hypoventilation.

Acetates↗

Analysis of increased myocardial contractility during sodium acetate infusion in humans.

To analyze the reported effects of acetate on left ventricular (LV) contractility during dialysis, LV function was studied before and after a 20-min sodium acetate (Na Ac) infusion (0.06 mmoles X kg-1 X min-1) in seven patients with heart rate (HR) controlled by atrial pacing. Angiographically determined LV volumes and LV pressures were used to calculate the LV function indices. A plasma acetate concentration of 3.13 +/- 1.05 (SD) mmoles X liter-1 induced an increase in cardiac index from 3.8 +/- 0.6 to 4.4 +/- 0.6 (SD) liter X min-1 X m-2 (P less than 0.01) and a rise in total body O2 consumption from 7.47 +/- 1.28 to 8.67 +/- 1.66 mmoles X min-1 X m-2 (P less than 0.05); there was no alteration of the volume elastic constant, of the end diastolic stress, and of the end systolic stress. There was an increase of the ejection fraction from 0.44 +/- 0.10 to 0.51 +/- 0.09 (P less than 0.01), the maximum velocity of shortening (Vmax, sec-1) from 1.37 +/- 0.25 to 1.55 +/- 0.28 (P less than 0.05), and of the end systolic stress-end systolic volume ratio (g X cm-2 X ml-1) from 2.99 +/- 0.76 to 3.40 +/- 0.98 (P less than 0.01). Hence, the enhancement of these indices was not the consequence of any alteration of HR, preload, or afterload.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗

Electrochemical heterogeneity of the cochlear endolymph: effect of acetazolamide.

The electrochemical composition of endolymph (EL) of two adjacent cochlear turns was studied in anesthetized rats. Differences in [K]EL, [Cl]EL, and endocochlear potential (EP) were found between the basal turn (165.6 +/- 3.0 mM, n = 14; 144.6 +/- 2.1 mM, n = 14;96.6 +/- 1.9 mV, n = 5, respectively) and the middle turn (155.7 +/- 2.5 mM, n = 15; 133.2 +/- 1.5 mM, n = 15; 87.0 +/- 1.6 mV, n = 6, respectively). The pH values of inner ear fluids were evaluated with 5,5-dimethyloxazolidine-2,4-dione: EL pH of either turn was not different from blood and perilymph (PL) pH. Acetazolamide (40 mg X kg body wt-1) reduced EP and [Cl]EL at each turn by about 20 and 6%, respectively, but [K]EL was unchanged. The electrochemical differences between the two turns persisted. Acetazolamide produced a 0.2-unit decrease in blood pH while the pH values of EL and PL remained unchanged. These results suggest the existence of an electrochemical gradient within EL from the base to the apex of the cochlea involving K+ and Cl- concentrations. H+ and HCO-3 do not appear to participate in this gradient, and the acid-base status in EL could be maintained both by active H+ transport into EL and by HCO-3 formation in the cochlear epithelium.

Acetazolamide↗

PTH-like glucagon stimulation of Ca and Mg reabsorption in Henle's loop of the rat.

The effects of glucagon and PTH on renal tubular electrolyte handling were studied in anesthetized, thyroparathyroidectomized Brattleboro rats infused with somatostatin. Fractional excretion of Ca and Mg was significantly lower during infusion of both hormones. Micropunctures of same nephrons localized the bulk of the increase in reabsorption in Henle's loop, where both hormones significantly enhanced the reabsorptive capacities for Ca, Mg, and K. Beyond the early distal tubule, Ca and Mg reabsorption was significantly greater during glucagon infusion and Ca reabsorption was significantly greater during PTH infusion. Cyclic adenosine monophosphate at a plasma concentration of 10(-6) M did not reproduce the effects of either glucagon or PTH. These results are similar to the findings reported for the effects of ADH and calcitonin on Ca, Mg, and K tubular handling, but different as far as Na and Cl are concerned, since their loop reabsorption was not significantly altered by glucagon and PTH. The data obtained here for glucagon and PTH, together with those for ADH and calcitonin, support the hypothesis that these four hormones exert similar effects in the thick ascending limb.

Absorption↗

Inter- and intracompartmental osmotic gradients within the rat cochlea.

The osmolality and the electrochemical composition of the endolymph, a potassium-rich positively polarized extracellular fluid in the cochlea, was studied in the rat. Endolymph of each cochlear turn was hyperosmotic to perilymph and plasma. Osmolalities (mosmol/kg H2O) were 329 +/- 2.9 (mean +/- SE) (n = 13) in basal turn endolymph, 322 +/- 2.7 (n = 9) in middle turn endolymph, 317 +/- 5.2 (n = 3) in apical turn endolymph, 289 +/- 3.1 (n = 14) in perilymph of the scala vestibuli, and 298 +/- 1.8 (n = 7) in plasma. Moreover, differences in osmolality and electrochemical composition of endolymph, involving resting potential and K and Cl concentrations, were observed between the basal and the middle cochlear turns, suggesting the presence of an electrical and osmotic gradient within endolymph, declining from the base to the apex of the cochlea. The active potassium transport into endolymph, located presumably in the stria vascularis, could account for both the internal and external osmotic gradients.

Animals↗

Ethacrynic acid facilitates gentamicin entry into endolymph of the rat.

Influence of ethacrynic acid (EA) upon gentamicin kinetics in perilymph and endolymph was studied in rats that were given a constant-infusion of gentamicin (150 micrograms/min) and EA (140 micrograms/min). Inner ear fluids and plasma were sampled up to 5 h. The purity of the endolymph was ensured by measurement of sodium and potassium concentrations. Gentamicin assay was done with a modified radioimmunoassay. Results show that EA facilitates the entry of gentamicin into endolymph, while it does not affect the kinetics of the drug in perilymph. Although the mechanism of this facilitation remains unclear, this result may account for the ototoxic potentiation reported between EA and aminoglycoside antibiotics.

Animals↗

Gentamicin persistence in rat endolymph and perilymph after a two-day constant infusion.

The kinetics of gentamicin in the inner ear fluids of rats were studied up to 15 days after cessation of a 2-day constant infusion of 10 micrograms/min. In endolymph, the concentration of gentamicin persisted at about 1 microgram/ml for up to 15 days, precluding the determination of the half-life of the drug in this fluid. In perilymph, gentamicin cleared more slowly than after a shorter period of infusion. These results suggest that the tissues of the inner ear could bind the aminoglycoside and then slowly release it into the surrounding fluids.

Animals↗

Effect of glucagon on magnesium renal reabsorption in the rat.

The recent localization, in the rat, of a glucagon-sensitive adenylate cyclase in these segments where the bulk of calcium and magnesium is reabsorbed suggests an effect of this hormone on calcium and magnesium tubular transport. Renal tubular handling of calcium and magnesium as well as of sodium and phosphate was therefore studied by clearance methods in anesthetized rats, either intact or thyroparathyroidectomized (TPTX), infused with glucagon at a rate of 25 ng.min-1/100 g bw just after a priming dose of 2.5 micrograms. The hormone administration resulted in a significant decrease of absolute and fractional magnesium excretion (from 16.3 +/- 0.7% to 9.7 +/- 1.7% for intact rats and from 20.9 +/- 1.8% to 6.9 +/- 1.0% for TPTX rats), associated with the well-known increase in sodium and phosphate fractional excretion. Moreover, a small and transient decrease of calcium fractional excretion was observed concomitantly with a decrease of plasma calcium concentration. The significant increase in magnesium absolute reabsorption, observed whatever the filtered load and independently of PTH and calcitonin, may be an evidence for a direct tubular effect of glucagon.

Absorption↗

K, Cl, and H2O entry in endolymph, perilymph, and cerebrospinal fluid of the rat.

The kinetics of radioactive potassium, chloride, and water entry into endolymph, perilymph, and cerebrospinal fluid were studied after intravenous administration of tracers in anesthetized and nephrectomized rats. Samples of cochlear endolymph, perilymph of scala vestibuli, perilymph of scala tympani, and cisternal cerebrospinal fluid were obtained. The data showed: 1) a rapid turnover of water in endolymph, perilymph, and cerebrospinal fluid, since 3H2O equilibrated with plasma in a few minutes; 2) a slow entry of 42K and 36Cl in perilymph, since 36Cl equilibrated with plasma after 2 h and 42K did not at 6 h; 3) an extremely slow entry of 42K and 36Cl in endolymph, since no equilibrium with plasma was obtained within the 5 h of the experiments. The comparison of the compartmental analysis of our data with the results of other studies using perilymphatic perfusion of tracers indicated that perilymph rather than plasma may be considered as the precursor of endolymph.

Animals↗