1 6 . A C T I O N S OF H O R M O N E S
6 0 7
I V . A C T I O N OF C O R T I C O S T E R O I D S A N D A D R E N A L I N E
A. EFFECTS ON TISSUE A N D CELL C U L T U R E S
Experiments in which unorganized cells were exposed in vitro to
corticosteroids suggest that these substances have a direct action on the
treated cells.
Gagianut (1951) reported that the growth of rabbit fibroblasts was
inhibited by addition of adrenocortical hormones to the medium.
Ruskin, Pomerat and Roskin (1951) obtained a slight but significant
growth-inhibition in cultures from chick-embryo heart, spleen and
spinal cord treated with either cortisone acetate, cortisone tricarallytate
and cortisone sulphate. Cortisone acetate was found to be the most
effective compound and cortisone sulphate the least effective one. The
treated cells displayed distinct differences in sensitivity which diminished in the following order: heart fibroblasts, spleen cells and spinal
cord. The dose of cortisone acetate to produce a minimal inhibition
was 50-100 ftg/ml for heart explants, 100-200 /xg for spleen explants and
over 200 /xg for spinal cord. These doses were considerably higher than
those necessary to produce a comparable effect in vivo, a. finding which
suggests that the direct effect of the drug on cells may become activated
in the organism.
Ohtani (1955) obtained a marked reduction of growth in cultures
of chick-embryo heart and spleen exposed to cortisone acetate in doses
ranging from 25-500 /xg/ml, while very small doses (0*05-0-005 jtxg/ml)
enhanced the growth of both types of cells. This finding fits in well with
results of Grossfeld (1959) who investigated the influence of hydrocortisone on respiration and growth of L-cells and on fibroblasts from
freshly explanted chick-embryo heart. A dose of 125 /xg/ml of hydrocortisone caused a marked reduction of respiration combined with a
rise in anaerobic glycolysis in a suspension of L-cells. This was accompanied by a growth reduction of 4 0 % . Addition of smaller doses
(1-25 fxg/ml), on the other hand, was followed by a stimulation of
respiration.
In the freshly explanted chick heart-fibroblasts the larger doses of
hydrocortisone inhibited both cell proliferation and production of
hyaluronic acid, which could no longer be detected after one or two
changes of medium. Leslie (1952) showed that an intermediate concentration of cortisone (15 ^g/ml) did not impair cell multiplication
in embryonic-chick heart fibroblasts but that, if applied in combination with growth hormone, it counteracted the growth inhibitory
effect of this hormone, and produced a stimulation of growth instead.
In such cultures the cell number was increased 75 % over that of the
6 0 7
I V . A C T I O N OF C O R T I C O S T E R O I D S A N D A D R E N A L I N E
A. EFFECTS ON TISSUE A N D CELL C U L T U R E S
Experiments in which unorganized cells were exposed in vitro to
corticosteroids suggest that these substances have a direct action on the
treated cells.
Gagianut (1951) reported that the growth of rabbit fibroblasts was
inhibited by addition of adrenocortical hormones to the medium.
Ruskin, Pomerat and Roskin (1951) obtained a slight but significant
growth-inhibition in cultures from chick-embryo heart, spleen and
spinal cord treated with either cortisone acetate, cortisone tricarallytate
and cortisone sulphate. Cortisone acetate was found to be the most
effective compound and cortisone sulphate the least effective one. The
treated cells displayed distinct differences in sensitivity which diminished in the following order: heart fibroblasts, spleen cells and spinal
cord. The dose of cortisone acetate to produce a minimal inhibition
was 50-100 ftg/ml for heart explants, 100-200 /xg for spleen explants and
over 200 /xg for spinal cord. These doses were considerably higher than
those necessary to produce a comparable effect in vivo, a. finding which
suggests that the direct effect of the drug on cells may become activated
in the organism.
Ohtani (1955) obtained a marked reduction of growth in cultures
of chick-embryo heart and spleen exposed to cortisone acetate in doses
ranging from 25-500 /xg/ml, while very small doses (0*05-0-005 jtxg/ml)
enhanced the growth of both types of cells. This finding fits in well with
results of Grossfeld (1959) who investigated the influence of hydrocortisone on respiration and growth of L-cells and on fibroblasts from
freshly explanted chick-embryo heart. A dose of 125 /xg/ml of hydrocortisone caused a marked reduction of respiration combined with a
rise in anaerobic glycolysis in a suspension of L-cells. This was accompanied by a growth reduction of 4 0 % . Addition of smaller doses
(1-25 fxg/ml), on the other hand, was followed by a stimulation of
respiration.
In the freshly explanted chick heart-fibroblasts the larger doses of
hydrocortisone inhibited both cell proliferation and production of
hyaluronic acid, which could no longer be detected after one or two
changes of medium. Leslie (1952) showed that an intermediate concentration of cortisone (15 ^g/ml) did not impair cell multiplication
in embryonic-chick heart fibroblasts but that, if applied in combination with growth hormone, it counteracted the growth inhibitory
effect of this hormone, and produced a stimulation of growth instead.
In such cultures the cell number was increased 75 % over that of the