Mechanism of the Calorigenic Action of Catecholamines
275
calorigenic actions of catecholamines were not smaller in these pithed rats
than in awake control animals. The total paralysation of rats by curare was
also without influence on calorigenic action of adrenaline (Fig. 1).
The possible contribution of cardio-acceleration to the calorigenic action
of catecholamines was evaluated indirectly. Bilateral vagotomy in the rat
induced a lasting increase of blood pressure and heart rate and augmented
by 65 % the cardiac index of MEESMANN [4] which is said to be a suitable
indicator of cardiac oxygen consumption. 0.3 mg/kg adrenaline-a highly
calorigenic dose (see Fig. l)-increased cardiac index only by 30 %. Bilateral vagotomy, nevertheless, did not increase oxygen consumption of
anesthetized rats. Thus, increased cardiac work does not contribute essentially to the calorigenic effects of catecholamines in the rat.
28
03 mg/kg
f\drenailne i P./~;::::::~t\
I
'X,
I
'
/
~~'"
I
'x
j
~
--~
~
............. "
/
.~
~~.I
---x
26
20
i8L-L----~-----L----~----~~--~
-30
0
30
60
90
120
min
Fig. 1. Mean oxygen consumption of 12 anesthetized (e--e) and 8 anesthetized,
curarised, and artificially respirated rats (x- -x) after 0.3 mg/kg adrenaline i.p.
Catecholamine-induced restriction of skin blood-flow is said to increase
body temperature and thereby to augment metabolism [lJ. Increments of
body temperature after calorigenic doses of catecholamines ranged in our
experiments from 0.2 to 1.2°C. They did not precede, but rather followed
the increase of metabolism with a delay, and therefore are not the cause but
the consequence of energy release. In further experiments we raised ambient
temperature from 28° to 32.5 0C. This effect increased the body temperature
of anesthetized rats as compared with control animals (28°C) by 1.2 °C, but
did not augment oxygen consumption (Fig. 2). The rise of oxygen consumption after adrenaline was also the same in both groups; again hyperthermia proved unimportant for the calorigenic action of catecholamines.
Our experiments demonstrate that catecholamine-induced hypermetabolism is a true increment of basal metabolic rate. The difficulties with
experiments in vitro probably result from the fact that sympathomimetic
calorigenesis is a consequence of metabolic events induced by sympathetic
glycogenolysis and lipolysis, namely lactic acid and fatty acid cycle. These
IS'
275
calorigenic actions of catecholamines were not smaller in these pithed rats
than in awake control animals. The total paralysation of rats by curare was
also without influence on calorigenic action of adrenaline (Fig. 1).
The possible contribution of cardio-acceleration to the calorigenic action
of catecholamines was evaluated indirectly. Bilateral vagotomy in the rat
induced a lasting increase of blood pressure and heart rate and augmented
by 65 % the cardiac index of MEESMANN [4] which is said to be a suitable
indicator of cardiac oxygen consumption. 0.3 mg/kg adrenaline-a highly
calorigenic dose (see Fig. l)-increased cardiac index only by 30 %. Bilateral vagotomy, nevertheless, did not increase oxygen consumption of
anesthetized rats. Thus, increased cardiac work does not contribute essentially to the calorigenic effects of catecholamines in the rat.
28
03 mg/kg
f\drenailne i P./~;::::::~t\
I
'X,
I
'
/
~~'"
I
'x
j
~
--~
~
............. "
/
.~
~~.I
---x
26
20
i8L-L----~-----L----~----~~--~
-30
0
30
60
90
120
min
Fig. 1. Mean oxygen consumption of 12 anesthetized (e--e) and 8 anesthetized,
curarised, and artificially respirated rats (x- -x) after 0.3 mg/kg adrenaline i.p.
Catecholamine-induced restriction of skin blood-flow is said to increase
body temperature and thereby to augment metabolism [lJ. Increments of
body temperature after calorigenic doses of catecholamines ranged in our
experiments from 0.2 to 1.2°C. They did not precede, but rather followed
the increase of metabolism with a delay, and therefore are not the cause but
the consequence of energy release. In further experiments we raised ambient
temperature from 28° to 32.5 0C. This effect increased the body temperature
of anesthetized rats as compared with control animals (28°C) by 1.2 °C, but
did not augment oxygen consumption (Fig. 2). The rise of oxygen consumption after adrenaline was also the same in both groups; again hyperthermia proved unimportant for the calorigenic action of catecholamines.
Our experiments demonstrate that catecholamine-induced hypermetabolism is a true increment of basal metabolic rate. The difficulties with
experiments in vitro probably result from the fact that sympathomimetic
calorigenesis is a consequence of metabolic events induced by sympathetic
glycogenolysis and lipolysis, namely lactic acid and fatty acid cycle. These
IS'