Læknablaðið : fylgirit - 01.09.1993, Blaðsíða 41

Læknablaðið : fylgirit - 01.09.1993, Blaðsíða 41
LÆKNABLAÐIÐ/FYLGIRIT 24 39 V 16 Gunnlaugur Claessen, 1881-1948: Brautryöjandi röntgenfræða, kennari, fræðari, vísindamaður Ásmundur Brekkan, prófessor. Myndgreiningadeild Landspítalans. Gunnlaugur Claessen fæddist 3. desember 1881. Hann lauk stúdentsprófi í Reykjavík 1901 og stundaði síðan læknisnám í Kaupmannahöfn. Að loknu kandidatsprófi stundaði hann framhaldsnám í röntgenstörfum í Stokkhólmi og Kaupmannahöfn, en sneri til íslands síðla árs 1913. Hann átti frumkvæði að og skipulagði Röntgendeild Landspítalans sem tók til starfa í desember 1930. Á spjöldum þessum er ferli og störfum Gunnlaugs á sviði röntgengreiningar og geislalækninga gerð nokkur skil í myndum og máh, en auk brautryðjandastarfs í sjúkdómsgreiningu, lækningu, kennslu og vísindum var hann mikilvirkur á íjölmörgum öðmm sviðum íslensks þjóðlífs. Gunnlaugur Claessen lést 15. júlí 1948. Mobilization of Calcium into the Cytosolic Compartment of Isolated Cardiac Ventricular Myocytes from the Rat: Response to Electrical Stimulation and Inotropic Agents. /O.G. B.1*orns- son, A.P. Thomas, I.R. Siemens, J.R. William- son. Metab. Res. Lab., Radcliffe Inf. Oxford, Dept. Biochem.fc Biophys. U. of Penn. U.S.A. The Ca2+ chelator fura-2 was used to con- tinuously monitor [Ca2+]i in isolated rat cardiac ventricular myocytes during the cell excitation/contraction cycle induced by el- ectrical stimulation. Brief electrical pulses (10 ms) caused a rapid and transient increase in [Ca2+]i (cell suspension: to.5_on = 13.5 ± 0.4 ms; to.5”Off = 224.4 ± 22.8 ms, n = 30, S£M). During electrical stimulation in either single cell preparations or in bulk cell sus- pensions, [Ca2+]i usually rose to peak levels which were two- or four-fold above resting levels (cell suspensions, resting [Ca2+]i = 69 ± 5 nmol/1, single cells, 81 ± 4 nmol/1, n = 30). There was a full recovery in [Ca2+]i between electrical pulses at a stimulation rate <: 0.2 Hz; however, stimulated at > 0.2 Hz, there was an upward shift in resting lev- els of [Ca2+]i, indicating an accumulation of Ca2+ within the cells. The rate of rise of the Ca2+ transients was independent of the fura-2 load, but the rate of decline and the peak height, as well as resting [Ca2+]i, decreased with increasing load of fura-2. Fura-2 bound Ca2+ increased with increasing fura-2 load, while protein-bound Ca2+ decreased. Ca2+ mob- ilization into the cytosolic compartment upon electrical stimulation was not affected by fura-2 (average 83 ± 5 pmol/mg protein), ex- cept at very high chelator load (> 300 pmol/ mg), where Ca2+ mobilization was increased. Elevating K+ of the medium depolarized the cells and caused a sustained increase in [Ca2+]i, the increase being primarily main- tained by flux of extracellular Ca2+ into the cells. The effect of potassium was enhanced by BAY K 8644 but suppressed by verapamil, ryanodine, or caffeine, and totally abolished by EGTA. The sodium channel activator vera- tridine depolarized the sarcolemma and in creased [Ca2+]i; tetrodotoxin suppressed this effect. Replacement of buffer Na+ with Li+ (to prevent Na+/Ca2+ exchange) elevated rest- ing [Ca2+]i, increased the calcium mobilizing effect of caffeine, and greatly decreased the rate of decline of [Ca2+]i following either caffeine treatment, or a train of electrical stimulations. A return of Na+ to the incub- ation buffer led to a rapid fall in [Ca2+]i to resting levels, even though changes in [Ca2+]i occurred at nanomolar levels only.- Fura-2 can be used to monitor fluxes of Ca2+ in myocytes. However, this chelator buffers and distorts the [Ca2+]i signal, especially during cell excitation, when [Ca2+]i changes may be large and occur rapidly, and calcium may become trapped inside the cells due to binding to the fluorescence indicator.

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