Læknablaðið : fylgirit - 01.09.1993, Síða 41

LÆKNABLAÐIÐ/FYLGIRIT 24
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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.