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A Loiseau

Publications and source records attributed to A Loiseau.

At least 37 records · Page 2Linked to original sources
PubMed1999

[Left ventricular performance, ventriculo-arterial coupling and mechanical output in hypertensive patients with and without left ventricular hypertrophy].

Left ventricular hypertrophy (LVH) is a physiological process of adaptation of the heart to mechanical load increase. Despite depression of left ventricular (LV) contractile performance, work efficiency is preserved and ventriculoarterial coupling is almost normal in hypertensive patients with LVH. To assess the differences between patients with and without LVH, LV contractile performance, the ventriculoarterial coupling and mechanical efficiency were compared in 2 groups of hypertensive patients with similar body surface area and arterial pressures, 23 without LVH (group 1) and 30 with LVH (group 2) and compared to data of 20 normotensive subjects. Left ventricular angiography coupled with simultaneous recording of pressures with micromanometer were used to determine end-systolic stress-to-volume ratio (ESSVR), end-systolic elastance (Ees), effective arterial elastance (Ea), external work (EW) and pressure-volume area (PVA). Left ventricular contractile performance assessed by Ees/100 g myocardial mass and EESVR were lower in group 2 than in group 1 (1.23 +/- 0.28 vs 1.89 +/- 0.48 mmHg/mL/100 g and 6.22 +/- 1.07 vs 9.56 +/- 0.97 g/cm2/mL/m2, respectively, both p < 0.0001, control subjects: 1.47 +/- 0.41 and 6.97 +/- 1.22, respectively). Ventriculoarterial coupling evaluated through Ea/Ees ratio (0.51 +/- 0.05 in group 1 vs 0.53 +/- 0.08 in group 2, 0.49 +/- 0.09 in control subjects), and work efficiency evaluated through EW/PVA ratio (0.80 +/- 0.02 in group 1 vs 0.78 +/- 0.03 in group 2, 0.80 +/- 0.03 in control subjects), were similar in the 2 groups and were comparable to control subject values. In conclusion, this study shows that ventriculoarterial coupling and work efficiency are comparable in hypertensive patients with and without LVH. These results suggest that in patients without LVH the matching between left ventricle and arterial receptor is preserved through an enhancement of myocardial contractility which is energetically costly. Conversely, LVH seems to be a useful adaptation which minimizes the energetical cost of high pressure generation.

Biomechanical Phenomena↗
PubMed1998

Left ventricular contractile performance, ventriculoarterial coupling, and left ventricular efficiency in hypertensive patients with left ventricular hypertrophy.

Contractile performance of hypertrophied left ventricle may be depressed in arterial hypertension. Ventriculoarterial coupling is impaired when myocardial contractile performance is reduced and when afterload is increased. The left ventricular contractile performance and the ventriculoarterial coupling were evaluated in 30 hypertensive patients with moderate left ventricular hypertrophy and 20 control subjects. Left ventricular angiography coupled with the simultaneous recording of pressures with a micromanometer were used to determine end-systolic stress/volume index, the slope of end-systolic pressure-volume relationship, ie, end-systolic elastance, effective arterial elastance, external work, and pressure-volume area. In hypertensive patients, left ventricular contractile performance, as assessed by end-systolic elastance/ 100 g myocardial mass, was depressed (4.35 +/- 1.13 v 5.21 +/- 1.89 mm Hg/mL/100 g in control subjects P < .02), when end-systolic stress-to-volume ratio was comparable in the two groups (3.85 +/- 0.99 g/cm2/mL in hypertensive patients versus 3.51 +/- 0.77 g/cm2/mL in control subjects). Ventriculoarterial coupling, evaluated through effective arterial elastance/end-systolic elastance ratio, was slightly higher in hypertensive patients (0.53 +/- 0.08 v 0.48 +/- 0.09 mm Hg/mL in control subjects, P < .05), and work efficiency (external work/pressure-volume area) was similar in the two groups (0.78 +/- 0.04 mm Hg/mL in hypertensive patients versus 0.80 +/- 0.03 mm Hg/mL in control subjects). This study shows that despite a slight depression of left ventricular contractile performance, work efficiency is preserved and ventriculoarterial coupling is almost normal in hypertensive patients with left ventricular hypertrophy. Thus, it appears that left ventricular hypertrophy might be a useful means of preserving the match between left ventricle and arterial receptor with minimal energy cost.

Arteries↗
PubMed1998

Effect of locally applied drugs on the endolymphatic sac potential.

In Ménière's disease, an inner ear disorder related to an endolymphatic hydrops, an alteration of the functioning of the endolymphatic sac has been proposed. The endolymphatic sac is assumed to be involved in the secretion/resorption of endolymph. The epithelial transport systems have been indirectly studied by the recording of the endolymphatic sac transepithelial potential (ESP) in control conditions and after the local injection of drugs such as diuretics that have been proposed in the treatment of Ménière's disease. The ESP was recorded, in vivo, in guinea pigs up to 150 minutes after the perisaccular injection of 5 microL of a 150 mmol/L (mM) NaCl solution containing various drugs known to inhibit ionic transport systems. The initial ESP was +8.4+/-0.3 mV (mean +/- SEM, n = 78). The basolateral injection of 5 microL of 150 mM NaCl induced an ESP decrease of 64%+/-6.0% (n = 12), 5 minutes after the end of the injection. Then ESP increased, returning to its initial value at 60 minutes and surpassing it at 120 minutes. Diuretics such as acetazolamide (10[-3] mol/L [M]), an inhibitor of carbonic anhydrase, and amiloride (10[-4] M), an inhibitor of Na channel or Na/H exchanger, decreased the ESP recovery. At variance, bumetanide (10[-6] M, 10[-4] M), the Na-K-Cl cotransport inhibitor, and chlorothiazide (10[-4] M), a Na-Cl cotransporter inhibitor, failed to alter the ESP as compared with the control group. Ouabain (10[-3] M), the Na+,K+-adenosine triphosphatase (ATPase) inhibitor, prevented the ESP recovery otherwise observed 60 minutes after the NaCl injection. Bafilomycin A1, the inhibitor of the vacuolar-type H+-ATPase, prevented the recovery of the ESP with a log-dose/effect (10[-5] M, 10[-6] M, 10[-8] M). Disulfonic acid stilbene (DIDS) (10[-4] M), an inhibitor of transporters involving HCO3-, also prevented the ESP recovery. These results suggest that the genesis of the ESP was highly dependent on acid-base transport systems including carbonic anhydrase, a vacuolar-type H+-ATPase, and an anionic transport system blocked by DIDS. Further studies are needed to confirm the alteration of the acid-base balance in this epithelium and its possible involvement in the pathogenesis of Ménière's disease.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1997

Potassium transport in opossum kidney cells: effects of Na-selective and K-selective ionizable cryptands, and of valinomycin, FCCP and nystatin.

The effects of two ionizable cryptands, the Na-selective (221)C10 and the K-selective (222)C10, and of valinomycin, FCCP and nystatin on K+ fluxes in opossum kidney (OK) cells have been quantified. The Na,K-ATPase (ouabain-sensitive 86Rb influx) was stimulated by nystatin (> or = 20%), and inhibited by the other ionophores (50-80%), by barium (K-channel blocker) (61%) and by amiloride (Na entry blocker) (34%). The Vmax of the Na,K-ATPase phosphatase activity was unmodified by the ionophores, indicating the absence of direct interaction with the enzyme. The ATPi content was unmodified by the inhibitors and nystatin, but was lowered by (221)C10 (47%), (222)C10 (75%), valinomycin (72%) and FCCP (88%). Amiloride was found to partially remove the inhibition caused by (222)C10 (51%) and valinomycin (49%). Rb efflux was stimulated by nystatin (32%), unmodified by valinomycin, and was inhibited by (221)C10 (19%), (222)C10 (19%) and FCCP (10%). Barium (39%) and amiloride (32%) inhibited this efflux and, in their presence, the nystatin effect persisted, whereas that of the other ionophores vanished. At pH 6.4, the Rb efflux decreased by 14% of its value at pH 7.4, with no additional inhibition by cryptands. Cryptands are shown to inhibit the pH-sensitive K+-conductance, probably by inducing a K+-H+ exchange at the plasma membrane, and by uncoupling oxidative phosphorylation by inducing the entry of K+ and H+ (and possibly Ca2+) ions into the mitochondria.

Adenosine Triphosphate↗
PubMed1997

Ventriculoarterial coupling and left ventricular efficiency in heart transplant recipients.

BACKGROUND: In heart transplants, left ventricular function may be impaired in the absence of rejection or graft atherosclerosis. Matching between left ventricle and arterial receptor, i.e., ventriculoarterial coupling, and left ventricular efficiency have never been studied. METHODS: Left ventricular pressure-volume loops and single beat analysis were used to determine effective arterial elastance (Ea) and the slope of the end-systolic pressure-volume relation (end-systolic elastance; Ees). Left ventricular efficiency was evaluated by determination of external work (EW), pressure-volume area (PVA), coronary blood flow (continuous thermodilution), and myocardial oxygen consumption (MVO2). Measurements were made at baseline in 11 control subjects and 9 heart transplant recipients (HTX) without rejection and were repeated after phenylephrine in the latter group. RESULTS: At baseline, Ees, Ees/Ea, and work efficiency (EW/PVA) were lower in HTX than in control subjects (2.51+/-0.87 vs. 3.70+/-1.15 mmHg/ml/m2, P<0.01; 0.96+/-0.21 vs. 1.47+/-0.31, P<0.001; and 0.53+/-0.08 vs. 0.59+/-0.09, P<0.01, respectively). Energy conversion efficiency (PVA/MVO2) and mechanical efficiency (EW/ MVO2) were higher in HTX (0.58+/-0.08 vs. 0.45+/-0.14, P<0.001; and 0.31+/-0.05 vs. 0.26+/-0.06, P<0.001, respectively). In HTX, phenylephrine infusion increased Ees, Ea, EW, PVA, and MVO2 without modifying Ees/Ea, EW/PVA, PVA/MVO2, and EW/MVO2. CONCLUSIONS: In heart transplants, (1) left ventricular contractility is moderately depressed; (2) elevation of energy conversion efficiency compensates for the decrease in work efficiency, allowing normal mechanical efficiency; and (3) alpha 1 adrenergic stimulation does not impair ventriculoarterial coupling and mechanical efficiency.

Adult↗
PubMed1997

[Ventriculoarterial coupling and left ventricular performance in hypertensive patients with left ventricular hypertrophy].

UNLABELLED: It has been shown that 1) contractile performance of hypertrophied left ventricle (LV) of hypertensive patients (HP) is depressed, and 2) ventriculoarterial (VA) coupling is altered when myocardial contractile performance is reduced and when afterload is increased. To assess the relationship between contractile performance of hypertrophied LV and the VA coupling in hypertensive patients. LV angiography coupled with simultaneous recording of pressures with micromanometer were used to determine end-systolic stress/volume index ratio (ESS/ESVi), the slope of end-systolic pressure-volume relationship, i.e. end-systolic elastance (Ees), effective arterial elastance (Ea), external work (EW) and pressure-volume area (PVA). Comparison of results in 30 HP and 20 control subjects (CS) showed that LV contractile performance assessed by Ees/100 g left ventricular myocardial mass (LVM, echocardiographic determination) was depressed (HT: 4.35 +/- 1.13; CS: 5.21 +/- 1.89 mmHg/ml/100 g; p < 0.02) and was negatively correlated to the LVM (Ees = -0.026 LVM + 3.363; r = 0.581; p < 0.001), when ESS/ESVi, another estimate of LV contractile performance, was comparable in the 2 groups (6.66 +/- 1.55 g/cm2/ml/m2 in HT vs 6.72 +/- 1.36 in CS; NS) and negatively correlated with the LVM (ESS/ESVi = -0.019 LVM + 8.947; r = 0.369; p < 0.01). Ventriculoarterial coupling evaluated through Ea/Ees ratio (Ea and Ees in mmHg/ml/m2) was slightly higher in HT (0.53 +/- 0.08 vs 0.48 +/- 0.09 in CS; p < 0.05), work efficiency (EW/PVA) was similar in the 2 groups (0.78 +/- 0.04 in HP vs 0.80 +/- 0.03 in CS) and PVA, which is representative of the myocardial oxygen demand per beat, is negatively related to LVM (PVA = -0.003 MVG + 1.44; r = 0.434; p < 0.01). CONCLUSIONS: this study shows that despite a slight depression of LV contractile performance, work efficiency is preserved and ventriculoarterial coupling is almost normal in HP with LV hypertrophy. Thus, it appears that LV hypertrophy might be a useful means of preservation of matching LV and arterial receptor with minimal energetical cost.

Blood Pressure↗
PubMed1996

Inhibition of Na-K-ATPase activity after prolonged hypoxia in an alveolar epithelial cell line.

Exposure to alveolar hypoxia may induce acute pulmonary edema. Because the vectorial sodium transport by alveolar epithelium represents an important mechanism for alveolar edema clearance, we examined whether hypoxia affects Na-K-ATPase activity in cultured SV40-transformed rat alveolar type II cells (SV40 ATII cells). Hypoxic exposures (O or 5% O2 for at least 12 h) induced a time- and O2 concentration-dependent decrease in ouabain-sensitive rubidium (osRb) influx. Neither the sensitivity of Rb influx to ouabain nor the maximum velocity of the enzyme measured on crude cell homogenates was affected by hypoxia. The osRb influx decrease was independent of hypoxia-induced ATP depletion. Na-K-ATPase inhibition was most likely related to impaired calcium homeostasis, because 1) calcium influx was increased in hypoxic cells, 2) hypoxia-induced osRb influx decrease was completely prevented by nifedipine (10-5 M), and 3) osRb influx decreased in normoxic cells incubated with ionomycin (10-6 M, 15 min). Furthermore, hypoxia-induced Na-K-ATPase impairment might be due, at least in part, to the endogenous release by hypoxic cells of a lipidic factor in extracellular medium, because incubation of normoxic cells with hypoxic cells conditioned medium (CM), or with the lipidic subphase from hypoxic cells CM, also induced a partial decrease in osRb influx. This decrease was associated with increased calcium influx into normoxic cells and was suppressed either by the removal of external calcium or by nifedipine, suggesting that the lipidic factor exerted its inhibitory action on Na-K-ATPase via an enhancement of calcium entry. These results indicate that prolonged hypoxic exposure impairs Na-K-ATPase activity in SV40 ATII cells and may therefore decrease the vectorial sodium transport by alveolar epithelium.

Adenosine Triphosphate↗
PubMed1995

Transport of competing Na and K ions by (222) C10-cryptand, an ionizable mobile carrier: effects of pH and temperature.

The kinetics of the electroneutral exchange of competing sodium and potassium with protons across the membrane of large unilamellar vesicles (LUV) were determined at two pH values when transport was induced by the simultaneous presence of (222)C10-cryptand and FCCP (proton carrier) at various temperatures. The aim of the present work was to quantify the pH-dependent enthalpies of an ionizable mobile carrier affinities for competing alkali cations, and to focus on the effects of pH and temperature on the competitive transport selectivity of the carrier for K+ over Na+ ions. At any given temperature and pH, the apparent pH-dependent affinity of (222)C10 was higher for K+ than for Na+. The enthalpy of this affinity for K+ was significantly lower than that for Na+, whereas it varied similarly with the pH (delta H(KpHmK) = 32.8 and 37.0 kJ/mol, and delta H(KpHmNa) = 47.9 and 52.9 kJ/mol at pH 7.8 and 8.8, respectively). When using a kinetic model, the pH effect on these parameters was discriminated (delta H(KmK) = 37.9 kJ/mol and delta H(KmNa) = 53.9 kJ/mol). The pH-dependence of the delta H(KpHm) of the cations could therefore theoretically be shown to arise from the temperature-induced changes in the ionization of the buffer dissolved in the aqueous phases and of the amine groups of the binding cavity of the carrier. The K/Na competitive transport selectivity (Sc(K/Na)) of (222)C10 increased linearly with the K+ concentration. It decreased hyperbolically with increasing concentration of Na+ while being independent of pH at any given temperature. In equimolecular ionic mixtures, Sc(K/Na) varied from 2.2 to 3.0 when temperature rose from 20 degrees C to 35 degrees C (delta H(Sc(K/Na)) = 15.6 +/- 0.5 kJ/mol). The results are discussed in terms of the structural, physico-chemical and electrical characteristics of carriers and complexes.

Bridged Bicyclo Compounds, Heterocyclic↗
PubMed1995

Na/K competitive transport selectivity of (221)C10-cryptand: effects of pH and carrier concentration.

The kinetics of the competitive transport of Na+ and K+ ions across the membrane of large unilamellar vesicles (LUV) were determined when transport was induced by (221)C10-cryptand, an ionizable mobile carrier. The experiments were performed at various pH values (7.7 and 8.7) and carrier concentrations (0.1, 0.5 and 1.0 microM) in order to quantify the effects of these parameters on the Na/K competitive transport selectivity of this mobile carrier. At any given pH and carrier concentration, the apparent affinity of (221)C10 for Na+ was higher and less dependent on the concentration of the other competing ion than that for K+. The Na/K competitive transport selectivity (SC(Na/K)) of (221)C10 increased linearly with the Na+ concentrations, decreased hyperbolically with increasing those of K+ and was independent of the pH and of the carrier concentration. In equimolecular ionic mixtures, this competitive selectivity amounted to about 1.5 and when the pH rose, the carrier selectivity for Na+ over K+ ions was enhanced by cation competition compared to transport of cations as unique substrates. Equations were established to describe the variations of the competitive transport selectivity (SC) of cryptands, and for comparison of their noncompetitive selectivity (SNC), with the ionic concentrations, the Michaelis parameters of the cations and the pH. The reaction order in Na+ (n(Na)) increased significantly with decreasing the pH and the K+ concentration. The results are discussed in terms of the structural, physico-chemical and electrical characteristics of carriers and complexes.

Binding, Competitive↗
PubMed1995

Evidence for Na-K-Cl cotransport in alveolar epithelial cells: effect of phorbol ester and osmotic stress.

We have investigated the presence of Na-K-Cl cotransport in alveolar type II cells using uptake of 86Rb. Several data support the presence of a Na-K-Cl cotransport in these cells. First, a large fraction of ouabain-resistant 86Rb uptake was inhibited by bumetanide and furosemide. Second, bumetanide-sensitive 86Rb uptake required the presence of Na+ and Cl- in the incubation medium; dependency on extracellular Na+ and K+ was hyperbolic, with a Km of 14.6 mM and 8.3 mM, respectively, while dependency on extracellular Cl- was sigmoidal, which suggests a 1:1:2 stoichiometry. Third, a fraction of amiloride-insensitive 22Na influx was deeply inhibited by bumetanide. 22Na influx was dependent on the presence of extracellular K+ and Cl-. Since Na-K-Cl activity dramatically decreased with time in culture, further characterization of the cotransport on polarized cells could not be performed. The phorbol ester PMA inhibited Na-K-Cl cotransport in a time- and concentration-dependent manner. This inhibition was mimicked by oleoylacetylglycerol, dioctanoylglycerol, and the diacylglycerol kinase inhibitor R59022, and was reversed by an antagonist of PKC, staurosporine. Since the Na-K-Cl cotransport has been reported to be involved in cell volume regulation, we investigated its modulation by changes in extracellular osmolarity. Na-K-Cl activity was increased after a two-step procedure: swelling in hypotonic medium followed by shrinking in hypertonic medium. Under these conditions, cotransport activity increased whenever PKC activity was up- or downregulated, which suggests that the cell volume-induced modulation of the cotransport is independent from the PKC activity. Though we were not able to determine the polarity of the cotransport, it may also be involved in the absorptive function of alveolar type II cells, and would provide an alternate pathway for sodium entry.

Animals↗
PubMed1995

CT assessment of bronchi in sarcoidosis: endoscopic and pathologic correlations.

PURPOSE: To evaluate the computed tomographic (CT) appearance of bronchi in patients with sarcoidosis and to correlate CT, endoscopy, and bronchial biopsy findings. MATERIALS AND METHODS: Sixty patients with sarcoidosis underwent CT and tracheobronchial endoscopy. CT findings of abnormalities of the bronchial walls and lumina were compared with endoscopic and biopsy findings. RESULTS: CT scans showed bronchial abnormalities in 39 patients (65%). CT and endoscopic findings were concordant in only 35 cases. However, CT showed abnormal lumina in 14 patients and endoscopy showed mucosal thickening in 12 of these 14 patients. CT findings of bronchial abnormalities were associated with the presence of bronchial granulomas (P < .0001). CT scans showed that, of the 37 patients with biopsy results of granulomatosis, 84% had thickened bronchial walls and 35% had luminal abnormalities. Eight CT findings were false-positive, and six were false-negative for the presence of granulomas. CONCLUSION: Bronchial involvement in sarcoidosis was detected at CT in 65% of cases. CT can help predict whether bronchial granulomas will be found in cases of sarcoidosis.

Adult↗
PubMed1995

Oxygen metabolites modulate sodium transport in gerbil middle ear epithelium: involvement of PGE2.

The middle ear epithelium and respiratory epithelia share basic properties such as homeostasis of air-filled cavities and mucociliary clearance toward the pharynx. With the middle ear SV40-transformed (MESV) cell line, we used the short-circuit current (Isc) technique to investigate changes in ion transport induced by oxidants. Xanthine and xanthine oxidase on the basal side of the monolayers dramatically increased Isc up to 50%. This effect was not affected by superoxide dismutase or mannitol, but could be blunted by catalase or 1,3-dimethyl-2-thiourea. Increasing concentrations of H2O2 from 10(-5) to 5 x 10(-4) M produced a dose-dependent increase in Isc from 0.26 +/- 0.16 up to 4.21 +/- 0.43 microA/cm2 (P < 0.05, n = 5). Concentration of half-maximal stimulation (EC50) was 4.68 x 10(-5) M. This effect was inhibited by indomethacin and was related to a sodium transport, since the H2O2-induced increase in Isc could be prevented or abolished by 1) apical addition of benzamil (10(-6)M) and 2) substitution of sodium with N-methyl-glucamine. H2O2 exposure also induced indomethacin-sensitive increase in released prostaglandin (PG) E2 (EC50 = 5.62 x 10(-5) M) and in cAMP content (EC50 = 3.95 x 10(-5) M) with similar kinetics. These results suggest that exposure of MESV cells to oxidants stimulates the production of PGE2, which in turn increases the transepithelial sodium transport rate.

Animals↗
PubMed1994

Na/K competitive transport selectivity of (221) C10-cryptand: effect of temperature.

The kinetics of the competitive transport of Na+ and K+ ions across the membrane of large unilamellar vesicles (LUV) were determined when transport was induced by (221)C10-cryptand at various temperatures in order to quantify the temperature-dependence of the Na/K competitive transport selectivity of this ionizable mobile carrier. At any given temperature, the apparent affinity of (221)C10 for Na+ was higher and less dependent on the concentration of the other competing ion than that for K+. Its enthalpy for Na+ (delta H(KmNa) = 50.6 kJ/mol) was not significantly different from that for K+ (delta H(KmK) = 52.7 kJ/mol). The Na/K competitive transport selectivity (SC(Na/K)) of (221)C10 increased linearly with the Na+ concentrations and decreased hyperbolically with increasing those of K+. When the cation concentrations were equal, this competitive selectivity amounted to about 2 at any given temperature. Equations were established to describe the variations of the competitive transport selectivity (SC) of cryptands, and for comparison of their noncompetitive selectivity (SNC), with the ionic concentrations and the Michaelis parameters of the cations. It is theoretically demonstrated that the ratio between the competitive and noncompetitive transport selectivities, i.e., SC/SNC, of mobile carriers does not depend on the Jmax of the competing ions and that its value amounts to 1 when the specific concentrations (C'S/Km) of the ions are equal. Under these conditions, the transport selectivity of any given mobile carrier has the same value whether determined from competition or separated experiments. The reaction order in Na+ (n(Na)) increased significantly as the temperature rose and decreased significantly as the K+ concentration increased. The results are discussed in terms of the structural, physicochemical and electrical characteristics of carriers and complexes.

Binding, Competitive↗
PubMed1994

Antidiuretic hormone restores the endolymphatic longitudinal K+ gradient in the Brattleboro rat cochlea.

In the cochlea, endolymph is hyperosmotic to plasma and perilymph. To test the hypothesis that antidiuretic hormone is involved in the modulation of endolymph secretion, the electrochemical composition of cochlear fluids, endolymph and perilymph, was studied in three groups of anaesthetized rats: control Long Evans rats, homozygous Brattleboro rats that are genetically deprived of antidiuretic hormone, and Brattleboro rats that were treated with antidiuretic hormone (dDAVP, 0.5 microgram/100 g body weight/24 h during 8 days). Endolymph was sampled from the scala media at each turn of the cochlea and perilymph from the scala vestibuli. In Long Evans rats, the endocochlear potential, the endolymphatic K+ and Cl- concentrations decreased from base to apex of the cochlea as previously reported in guinea pigs and Sprague Dawley rats. In Brattleboro rats, the endocochlear potential and the Cl- concentration gradients were still present, whereas the K+ concentration gradient were still present, whereas the K+ concentration gradient was absent. This K+ gradient was restored by the administration of dDAVP, which increased the K+ concentration at the base of the cochlea. This work indicates that the K+ secretion in endolymph, and thus the osmolality, may be locally modulated by the antidiuretic hormone, probably via V2 receptors.

Animals↗
PubMed1994

Ultrastructural alterations of the air-blood barrier in sarcoidosis and hypersensitivity pneumonitis and their relation to lung histopathology.

To evaluate the incidence of air-blood barrier lesions in the course of chronic interstitial lung diseases, we studied by electron microscopy open lung biopsy specimens from patients with sarcoidosis or chronic hypersensitivity pneumonitis, and compared the distribution of ultrastructural air-blood barrier lesions (including swelling or destruction of epithelial and endothelial cells, type II cell hyperplasia, and basement membrane disruption) with the type of histopathologic abnormalities present (including inflammation, inflammation and fibrosis, or fibrosis alone). Ultrastructural lesions of the air-blood barrier were frequently observed in sarcoidosis as well as hypersensitivity pneumonitis. Their nature and distribution were highly dependent on the histologic pattern of lung tissue in which they were present: epithelial and/or endothelial injury was more frequently observed in inflammatory areas (90 to 100% of all lung specimens displaying inflammation alone), whereas type II cell hyperplasia was mainly identified in fibrotic tissues (83 to 100% of all lung specimens displaying fibrosis alone). Strikingly, in lung tissue considered as normal by light microscopy, air-blood barrier was frequently found to be damaged (50 to 62% of apparently normal lung specimens), suggesting that alveolar lesions may constitute an early phenomenon in the course of pulmonary inflammatory processes. The air-blood barrier alterations observed in this study may provide an anatomic basis for the modifications of alveolar permeability described in pulmonary sarcoidosis and hypersensitivity pneumonitis.

Adult↗