[Multiple pulmonary artery aneurysms in Behcet's disease. Value of intravascular embolization].
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Biomedical subjects
Publications and source records attributed to F Lang.
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To gain some insight into electrogenic transport processes across the plasma membrane of Madin-Darby canine kidney (MDCK)-cells, continuous measurements of the potential difference across the plasma measurements of the potential difference across the plasma membrane (PD) were made during step changes of extracellular ion composition as well as application of barium or valinomycin. During control conditions mimicking in vivo extracellular fluid, PD approaches -51.5 +/- 0.8 mV (n = 62). Step increase of extracellular potassium concentration from 5.4 to 10, to 20 or to 35 mmol/l, depolarizes PD by +5.5 +/- 0.8 mV (n = 7), by +15.8 +/- 0.5 mV (n = 64) and by +23.8 +/- 1.2 mV (n = 12), respectively. 1 mmol/l barium depolarizes PD by +19.8 +/- 0.6 mV (n = 38) and abolishes the effect of increasing extracellular potassium from 5.4 to 10 mmol/l but not to 35 mmol/l. Ten mumol/l valinomycin hyperpolarizes PD to -69.3 +/- 2.9 mV (n = 7). In the presence of valinomycin, increase of extracellular potassium from 5.4 to 20 mmol/l depolarizes PD by +31.0 +/- 1.0 mV (n = 7). Ouabain depolarizes PD and reduces the sensitivity of PD to extracellular potassium concentration. Omission of extracellular bicarbonate and carbon dioxide as well as increase of extracellular bicarbonate at constant carbon dioxide lead to a hyperpolarization and enhanced sensitivity of PD to extracellular potassium. In the presence of barium, the effects of omitted bicarbonate and carbon dioxide of MDCK-cells is highly conductive to potassium.(ABSTRACT TRUNCATED AT 250 WORDS)
According to a previous study from this laboratory, the electrochemical gradient for potassium across the peritubular cell membrane of proximal tubules in the isolated perfused frog kidney increases following the application of ouabain. In order to test, if this phenomenon were due to a decrease of potassium conductance, the effects of ouabain on cell membrane resistances and the sensitivity of the peritubular cell membrane potential difference (PDpt) to step changes of peritubular potassium and bicarbonate concentration were studied. In the absence of ouabain, PDpt averaged -60 +/- 3 mV (n = 25). A step increase of peritubular potassium concentration from 3 to 18 mmol/l (pH 8.07) depolarizes PDpt (delta PDk) by +24 +/- mV (n = 8). An increase of bicarbonate from 20 to 40 mmol/l (pH 8.07) hyperpolarizes PDpt (delta PDb) by -2.8 +/- 0.4 mV (n = 9). The resistance of the luminal and peritubular cell membranes in parallel (Rm) amounts to 45 +/- 9 k omega cm (tubule length) (n = 4) and the voltage divider ratio (VDR) to 1.4 +/- 0.2 (n = 7). The resistance of the cellular cable (cellular core, Rc) approaches 131 +/- 37 M omega/cm (n = 4). Peritubular application of 0.1 mmol/l ouabain leads to a gradual decline of PDpt (t1/2 approx. 30 min), to an increase of Rm, a decrease of delta PDk and an increase of delta PDb. VDR and Rc are not changed significantly. The data point to a functional link between the sodium/potassium ATPase and the potassium conductance of the peritubular cell membrane.
The present study was designed to elucidate the effects of sodium-coupled transport on the electrical properties of proximal tubule cells in the isolated perfused frog kidney. Cable analysis techniques have been employed to determine the resistance of the luminal and peritubular cell membranes in parallel (Rm) and the apparent ratio of the luminal over the peritubular cell membrane resistance (VDR). Furthermore, the sensitivity of the potential difference across the peritubular cell membrane (PDpt) to 6-fold increases of peritubular potassium concentration (delta PDk) was taken as a measure of the relative potassium conductance of this membrane. In the absence of luminal phenylalanine, PDpt amounts to -60 +/- 1 mV (n = 90), Rm to 36 +/- 3 k omega cm (n = 22), VDR to 1.81 +/- 0.14 (n = 20), and delta PDk to 15.0 +/- 0.9 mV (n = 25). The application of 10 mmol/l phenylalanine replacing 10 mmol/l raffinose leads to a rapid (within 30 s) depolarisation of PDpt to 50 +/- 5% of its control value and to a delayed (within 12 min) recovery to 95 +/- 5% of control. The rapid depolarisation is associated with a decline of Rm and VDR, indicating a decrease mainly of the luminal cell membrane resistance. During recovery of PDpt there is a parallel increase of VDR and a further decline of Rm pointing to a decline of the basolateral cell membrane resistance. Delta PDk is decreased during rapid depolarisation but increases again during the recovery phase. Thus, phenylalanine initially decreases but then increases above control the apparent potassium conductance.(ABSTRACT TRUNCATED AT 250 WORDS)
The present study was performed to test the influence of sodium coupled transport of neutral substrates on intracellular pH and sodium activity in proximal tubules of the amphibian kidney. To this end, kidneys of rana esculenta have been isolated and perfused both through the portal vein (peritubular capillaries) and the aorta (luminal perfusate). The potential difference across the peritubular membrane of proximal tubule cells has been reduced with conventional (PDpt) as well as with sodium (PDna) and hydrogen ion (PDh) selective microelectrodes continuously before, during, and after the luminal application of 10 mmol/l phenylalanine, replacing 10 mmol/l raffinose. PDh and PDna allowed the calculation of intracellular pH (pHi) and sodium activity (Nai), respectively. In the absence of phenylalanine in the tubule lumen, PDpt approximates -57.5 +/- 2.3 mV (n = 27), pHi 7.73 +/- 0.04 (n = 14, extracellular pH 7.77), and Nai 13.3 +/- 0.9 mmol/l (n = 13, extracellular sodium activity 74 mmol/l). Within 1 min the luminal application of phenylalanine leads to a depolarisation of PDpt by +32 +/- 2 mV, as well as an increase of pHi by 0.24 +/- 0.04 and of Nai by 5.2 +/- 1.0 mmol/l. At 8 min from luminal application of phenylalanine, Nai plateaus 5 +/- 1 mmol/l above control value, PDpt increases again to a value of +12 +/- 2 mV below and pHi decreases to a value 0.04 +/- 0.07 above their respective control values. All changes are fully reversed after removal of phenylalanine from the tubule lumen.(ABSTRACT TRUNCATED AT 250 WORDS)
This study concerns the effect of a 12-day cyclosporin A (CsA) treatment (50 mg per kg per day) on "autoimmune" diabetes induced by 5 low doses (40 mg per kg per day) of streptozotocin (SZ). The SZ-treatment period was initiated 4 days after initial administration of CsA. In young (45-day) CD-1 male mice, CsA enhanced hyperglycemia, hypoinsulinemia and beta-cell destruction following a multiple low-dosage SZ. Moreover, CsA did not prevent development of insulitis induced concomitantly by SZ. Similarly, CsA enhanced the "toxic" diabetes produced by a single high dose (160 mg/kg) of SZ. Furthermore, in the absence of SZ, CsA alone induced glucose intolerance, associated with beta-cell degranulation and high pancreatic CsA content. The enhancement of SZ-induced diabetes by CsA may thus be due to toxicity of the immunosuppressive agent for pancreatic beta cells. This side effect is noteworthy because CsA is currently being used in the therapy of human insulin-dependent diabetes.
A 53-year-old man with hepatitis concurrent with cirrhosis was simultaneously positive for hepatitis B surface antigen and heterotypic anti HBs antibody. This could be explained by a state of tolerance, with chronic carrying of B virus (subtype a y w3), but would not preclude B virus (subtype d) reinfection, inducing the synthesis of specific anti-d antibodies. In the same patient, the very high level of 3460 ng/ml was reached for alpha-fetoprotein; this was transitory and returned to normal within 8 months; it was probably due to the acute hepatitis. Thus it appears that, even in cases of cirrhosis, a major rise in this marker does not absolutely imply the presence of hepatocellular carcinoma.
Using long-term automatic blood pressure recording it has previously been shown that subjects with family history of hypertension show a minute fall of blood pressure during sodium restriction, which is reversible by high sodium intake. Thus normotensives with hypertensive antecedents as a group are salt-sensitive, whereas normotensives without heredity of hypertension as a group are salt-resistant. The present study compares intracellular sodium, potassium and calcium, sodium pump activity, NaK-cotransport of red blood cells and density and affinity of alpha 2-adrenergic receptors of platelets in normotensive subjects classified according to family history of hypertension and according to 'salt sensitivity' and 'salt resistance'. Neither the family history of hypertension nor salt sensitivity correlated with intracellular sodium, potassium, calcium, Na-pump activity and NaK-cotransport. Alpha 2-adrenergic density was higher in salt-sensitive than in salt-resistant subjects (P < 0.05) but similar in subjects with a positive and negative family history of hypertension. However, alpha 2-adrenergic receptor density decreased significantly during 2 weeks of moderate salt restriction from 169.6 +/- 34.2 to 142.6 +/- 30.8 (P < 0.01, paired t-test), which may explain the decreased pressor response to infused noradrenaline observed in a previous study during moderate salt restriction. It is concluded that in humans there is no association of genetic predisposition of hypertension or of salt sensitivity to an alteration of sodium pump activity, NaK-cotransport, intracellular sodium and calcium. Alpha 2-receptor density of platelets deserves further study as a possible predictor of salt sensitivity in normotensives.
We report on two cases of angiodysplasia of the digestive tract complicated by serious acute bleeding. The preoperative diagnoses were made by angiography. One case concerned a voluminous jejunal lesion which was macroscopically visible; the other concerned a punctiform lesion detected only by angiography and not found on the pathology specimen. The authors insist on the potential gravity of these angiodysplastic lesions, the necessity to perform an emergency celio-mesenteric angiogram when confronted with a serious digestive tract hemorrhage non-explained by conventional methods of exploration when they can be performed.
The in vivo firing patterns of the fast closer excitor (FCE) and slow closer excitor (SCE) motoneurons to the dimorphic claws of the lobster Homarus americanus were analyzed during reflex closure activity by identifying postsynaptic potentials in muscle fibers with known motor innervation. Three types of claw activity were observed: slow closure, rapid closure, and maintained closure. Slow closure and rapid closure in both claws were mediated by SCE and FCE, respectively. In the cutter, maintained closure was mediated only by SCE; in the crusher, both FCE and SCE could maintain closure. The homologous SCEs displayed no significant differences in activity; in both claws, they fired at medium-to-high frequency. The homologous FCEs did display different spike frequencies during claw closure. The crusher FCE fired at high frequencies; the cutter FCE fired at much lower frequencies. Such in vivo differences in axon activity between homologous FCEs are correlated with claw dimorphism and with the population of muscle fiber types.
Using conventional and ion selective microelectrodes, the effect of ouabain (10(-4) mol/l) on peritubular cell membrane potential (PDpt), on intracellular pH (pHi) as well as on the intracellular ion activities of Cl- (Cli-), K+ (Ki+), Na+ (Nai+) and Ca2+ (Ca2i+) was studied in proximal tubules of the isolated perfused frog kidney. In the absence of ouabain (PDpt = -57.0 +/- 1.9 mV), the electrochemical potential difference of chloride (apparent mu Cl- = -22 +/- 2 mV) and of potassium (mu K+ = +24 +/- 3 mV) is directed from cell to bath, of H+ (mu H+ = -42 +/- 5 mV), of Na+ (mu Na+ = -102 +/- 4 mV) and of Ca2+ (mu Ca2+ = -148 +/- 6 mV) from bath to cell. Ouabain leads to a gradual decline of PDpt, which is reduced to half (PDpt, 1/2) within 31 +/- 4.6 min (in presence of luminal glucose and phenylalanine), and to a decline of the absolute values of apparent mu Cl+, of mu H+, mu Na+ and mu Ca2+. In contrast, an increase of mu K+ is observed. At PDpt, 1/2 apparent Cl-i increases by 6.2 +/- 1.0 mmol/l, pHi by 0.13 +/- 0.03, Ca2+i by 185 +/- 21 nmol/l, and Nai+ by 34.2 +/- 4.6 mmol/l, whereas Ki+ decreases by 37.7 +/- 2.2 mmol/l. The results suggest that the application of ouabain is followed by a decrease of peritubular cell membrane permeability to K+, by an accumulation of Ca2+, Na+ and HCO3- in the cell and by a dissipation of the electrochemical Cl- gradient.
Inhibition of basolateral Na+/K+ ATPase by ouabain eventually abolishes transport of glucose. The present study was performed to test, if this effect is due to a dissipation of the electrochemical gradient for sodium or due to a regulatory inhibition of sodium-coupled glucose entry across the luminal membrane at increasing intracellular sodium activity. To this end, proximal convoluted tubules of the doubly perfused isolated frog kidney were perfused alternatively with solutions containing either 5 mmol/l glucose or raffinose. The potential difference across the peritubular cell membrane (PDpt) and across the epithelium (PDte) has been recorded with conventional and across the peritubular cell membrane with ion selective microelectrodes (PDpt). In the absence of luminal glucose PDpt is (+/- SEM) -54.0 +/- 2.4 mV, PDte = -1.2 +/- 2.0 mV and PDNapt = -96 +/- 5 mV. The electrochemical gradient for sodium (mu Na+) amounts to 95 mV and intracellular sodium activity to 14 mmol/l (extracellular sodium activity is 74 mmol/l). Luminal application of glucose leads to a rapid depolarisation of PDpt (delta PDpt = 8.6 +/- 0.9 mV and PDNapt (delta PDNapt = 11.1 +/- 3.0 mV) and to hyperpolarisation of PDte (delta PDte = -0.8 +/- 0.2 mV). The peritubular application of ouabain leads to a gradual, reversible and proportional decline of PDpt, PDNapt and mu Na+. Glucose induced delta PDpt and delta PDNapt decrease in parallel to PDpt and PDNapt, resp. In a separate series, the lumped conductance (Gm) of the luminal and basolateral cell membrane has been determined, which amounts to 2.4 +/- 0.3 microS/mm (tubule length). Gm decreases 23 +/- 4%, when PDpt is decreased to half.(ABSTRACT TRUNCATED AT 250 WORDS)
Previous observations suggest that luminal application of tetra-N-alkylammonium ions may impair ion transport in the amphibian diluting segment. To investigate this question conventional KCl-filled and Cl- sensitive microelectrodes were applied in diluting segments of the isolated perfused kidney of rana esculenta to evaluate transepithelial electrical and chloride electrochemical (PDte, EClte) as well as peritubular cell membrane potential difference (PDpt), measured at static head conditions. After determination of control values the tubule lumen was exposed to choline (95 mmol/l, substituted for Na+) both in presence or absence of furosemide (5 X 10(-5) mol/l). Then, the lumen was again perfused with control solution and the measurements were repeated. Thus, a time course for possible choline induced effects was obtained both in the presence and absence of furosemide. The lumen positive PDte decreased from 11.2 +/- 1.0 mV to 6.3 +/- 0.8 mV after 2 min and to 1.9 +/- 0.4 mV after 30 min exposure to choline. PDpt (cell interior negative) decreased from 70 +/- 2 mV to 58 +/- 3 mV and to 42 +/- 5 mV after 2 and 30 min, respectively. Intraluminal Cl- activity increased from its initial steady state value of 20 +/- 2 mmol/l to 39 +/- 2 mmol/l after 30 min exposure to choline. However, if the tubule lumen was exposed to choline in presence of furosemide (5 X 10(-5) mol/l), all the above described choline-induced effects did not become apparent.(ABSTRACT TRUNCATED AT 250 WORDS)
Transepithelial H+ transport was studied in diluting segments of the isolated-perfused kidney of rana esculenta. The experiments were performed in controls as well as in K+-adapted and Na+-adapted animals (exposed to 50 mmol/l KCl or NaCl, resp. for at least 3 days). Conventional and single-barreled, liquid ion-exchanger H+-sensitive microelectrodes were applied in the tubule lumen to evaluate transepithelial H+ net flux (JHte) as well as limiting transepithelial electrical and H+ electrochemical potential differences (PDte, EHte) and luminal pH at zero net flux conditions. The measurements were made in absence (control) and presence of furosemide (5 X 10(-5) mol/l) or amiloride (10(-3) mol/l). EHte (lumen positive vs ground) was 19 +/- 3 mV in controls, 43 +/- 3 mV in K+ adapted but about zero in Na+ adapted animals. Using the corresponding PDte-values, steady state luminal pH of 7.63 +/- 0.05, 7.13 +/- 0.05 and 8.02 +/- 0.02 was calculated for the respective groups of animals (peritubular pH 7.80). In parallel, significant secretory JHte (from blood to lumen) was found in controls (14 +/- 2 pmol X cm-2 X s-1) which was stimulated by K+ adaptation (61 +/- 8 pmol X cm-2 X s-1) but reversed in direction by Na+-adaptation (-8 +/- 1 pmol X cm-2 X s-1). Amiloride inhibited secretory JHte.(ABSTRACT TRUNCATED AT 250 WORDS)
Manufacture, properties and use of a micro enzyme electrode for continuous monitoring of volume fluxes in the isolated tubule preparation is described. The specific electrode is a galactose-oxidase enzyme electrode, which can be used to detect changes in raffinose concentrations. The electrode's response to raffinose is almost linear over concentrations from 0-12 mmol/l. The electrode equally responds to galactose as to raffinose but is insensitive to other sugars, to pH changes (from 6.0-8.0), CO2 (from 1-10%) and electrolytes tested. Reducing O2 from 100 to 10% and to 1%, leads to a reduction of the reading by 10% and 30%, respectively. The reading is almost doubled when the temperature is increased from 20-40 degrees C. Furthermore, reducing agents such as uric acid and ascorbic acid interfere with the reading. If these substances and raffinose are omitted from the perfusate for isolated perfused proximal mouse tubules, the reading is identical in perfusate and collected fluid, indicating that the tubular epithelium does not produce substances in sufficient amounts to interfere with the electrode reading. After addition of 6 mmol/l raffinose to the perfusate the raffinose concentration in the collected fluid of 0.76 +/- 0.05 mm segments of straight proximal mouse tubules (perfusion rate = 3.4 +/- 0.45 nl/min) is 10.2 +/- 0.3 mmol/l, indicating a volume reabsorption of 1.5 +/- 0.3 nl/min. Peritubular application of acetazolamide reduces the volume reabsorption by 42 +/- 4%.
The design and application of a micro-plantinum electrode for continuous monitoring of reducing activity in the isolated tubule preparation is described. The electrodes response to H2O2 up to 0.1 mmol/l, to uric acid up to 0.3 mmol/l, ascorbic acid up to 1.0 mmol/l and cysteine up to 2.0 mmol/l is almost linear. The electrode is insensitive to extracellular ions, to changes of pH (5.5-8.0), CO2 (1-10%) and O2 (1-100%). The reading of the electrodes is almost doubled when the temperature is increased from 20-40 degrees C. When reducing substances are omitted from the perfusate for isolated perfused proximal tubules of the mouse, the reading is identical in perfusate and collected fluid, indicating that the tubular epithelium does not produce redox substances in sufficient amount to interfere with the electrode reading at flow rates approximately 10 nl/min. When the tubule is perfused with solutions containing 0.3 mmol/l uric acid, the uric acid concentration in the collected fluid is 0.16 +/- 0.01 mmol/l after a contact time of 1.36 +/- 0.1 S, revealing net uric acid reabsorption. Adding probenecid to the luminal perfusion fluid leads to a 37.5 +/- 1.0% increase of uric acid concentration in collected fluid, disclosing the inhibitory effect of probenecid on uric acid reabsorption. If 0.3 mmol/l uric acid is added to the bath, 0.017 +/- 0.002 mmol/l uric acid is detected in the luminal fluid. The entry of uric acid into the lumen is abolished by 10(-4) mol/l pyrazinamide.
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