Goodpasture's syndrome. Unusual presentation after exposure to hard metal dust.

An unusual case of Goodpasture's syndrome in a 26-year-old man with occupational exposure to hard metal dust is described. The patient developed a life-threatening interstitial lung disease that was followed by a rapidly progressive glomerulonephritis two months later. To our knowledge, association of Goodpasture's syndrome and hard metal exposure has not been reported previously.

Apparent chloride conductance of subconfluent Madin Darby canine kidney cells.

In incompletely confluent Madin Darby canine kidney (MDCK)-cells continuous measurements of the potential difference across the cell membrane (PD) were made with conventional microelectrodes during rapid changes of extracellular chloride concentration. During control conditions mimicking in vivo situation, PD averages -50.3 +/- 0.7 mV. Reduction of extracellular chloride concentration from 122 mmol/l to 64.5 mmol/l depolarizes the cell membrane by +1.8 +/- 0.2 mV while reduction to 16 mmol/l leads to a transient, variable depolarization followed by a hyperpolarization of the cell membrane by -11.8 +/- 1.4 mV. 1 mmol/l anthracene-9-COOH hyperpolarizes the cell membrane by -10.7 +/- 1.0 mV, and abolishes the effect of altered extracellular chloride concentration (-0.6 +/- 0.5 mV), 1 mumol/l diphenylamine-2-carboxylate hyperpolarizes the cell membrane by -11.7 +/- 1.4 mV. 10 mumol/l furosemide hyperpolarize the cell membrane by -11.4 +/- 1.4 mV. Step increases of extracellular potassium concentration from 5.4 to 20 mmol/l depolarize the cell membrane by +14.9 +/- 1.0 mV in the absence of inhibitors, by +24.2 +/- 1.3 mV in the presence of anthracene-9-COOH and by +28.8 +/- 0.7 mV in the presence of furosemide. 10 mumol/l isoproterenol depolarize the cell membrane by +2.4 +/- 0.3 mV and increase the depolarizing effect of reducing extracellular chloride concentration to 64.5 mmol/l (+2.9 +/- 0.4 mV). 1 mumol/l forskolin depolarizes the cell membrane by +5.8 +/- 1.0 mV. In conclusion, chloride conductance of subconfluent MDCK-cells may be small during control conditions, is apparently decreased by anthracene-9-COOH and reduction of extracellular chloride concentration but is enhanced by isoproterenol.

Effects of epinephrine on electrical properties of Madin-Darby canine kidney cells.

The present study has been performed, to test for the influence of epinephrine on the potential difference across the cell membrane (PD) of Madin-Darby canine kidney (MDCK) cells. Under control conditions, mimicking the in vivo situation, PD averages - 53.3 +/- 0.9 mV (n = 37). Increasing extracellular potassium concentration from 5.4 to 10 and 20 mmol/l depolarizes the cell membrane by +4.3 +/- 0.4 mV (n = 5) and +15.8 +/- 1.2 mV (n = 5), respectively. The application of 1 mumol/l epinephrine leads to sustained hyperpolarization of the cell membrane to -71.5 +/- 0.7 mV (n = 37). In the presence of epinephrine, increasing extracellular potassium concentration from 5.4 to 20 mmol/l depolarizes the cell membrane by +30.6 +/- 0.2 mV (n = 5); 1 mmol/l barium depolarizes the cell membrane by +14.8 +/- 0.7 mV (n = 20) and abolishes the effect of step increases of extracellular potassium concentration from 5.4 to 10 mmol/l. In the presence of barium, epinephrine leads to a transient hyperpolarization by -31.2 +/- 1.2 mV (n = 18). During this transient hyperpolarization, the cell membrane is sensitive to extracellular potassium concentration despite the continued presence of barium; 10 mumol/l verapamil depolarizes the cell membrane to -41.0 +/- 2.6 mV (n = 11). In the presence of verapamil, the hyperpolarizing effect of epinephrine is only transient; 10 mumol/l phentolamine depolarizes the cell membrane by +3.0 +/- 0.6 mV (n = 8). In the presence of phentolamine, the effect of epinephrine is virtually abolished (+0.4 +/- 0.6 mV, n = 8); 1 mumol/l isoproterenol depolarizes the cell membrane by +2.8 +/- 0.8 mV (n = 8).(ABSTRACT TRUNCATED AT 250 WORDS)