Heart Rate Adaptation to Temperature
99
factors (driving forces, coefficients and fluxes) in the pacemaker system that
influence the steady state transition of heart rate in capacity adaptation to
temperature? It is well known that heart frequency is a function of the rapidity of diastolic depolarisation of the pacemaker tissues, the rapidity being
a function of the ion diffusion potentials and the specific permeabilities.
According to NERNST'S law, diffusion potentials are dependent on the actual
ion concentration differences in- and outside the cell; they are real steady
state values. Of course, they are dependent on the active and passive ion
transport across the membrane. If the unidirectional passive sodium influx
is greater than the active transport from inside the cell to the intercellular
space, the sodium quotient Nao/Naj is lowered and a decrease of the heart
frequency results; reciprocal conditions hold true for the potassium potential.
The inactivation of acetylcholine at the membrane is increased by temperature more markedly than its rate of replenishment; permeability of
potassium depends on the actual concentration of acetylcholine. The
lowered permeability as a consequence of temperature rise increases the
rapidity of diastolic membrane-depolarization. In the time course of heart
frequency the balance of potassium transport will be shifted toward a
higher rate of active transport; whereas, because of frequent depolarizations, the balance of sodium transport is shifted towards a higher passive
influx rate. Thus, the higher temperature leads to a gradually increasing
potassium potential and a gradually decreasing sodium potential. Following
a rise in temperature, therefore, the heart rate will be lowered starting from
the first maximum-value; it will reach a steady state according to the new
ion transport-balance.
This briefly outlined hypothesis has been tested by experiments with
capacity adaptation after certain variations of permeability and ionic
potentials. This was done by adding to the perfusion medium of the heart
various substances, such as ACh, atropine, eserine, epinephrine and fJreceptor blocking agents. The ionic potentials have been varied by diminishing or increasing the concentration of extracellular sodium or potassium
(or chloride). Under these special circumstances, the steady state transitions
behaved exactly in the mode predicted by our hypothesis.
Finally we carried out another test in order to support the validity of the
hypothesis. At constant temperature the heart rate was doubled for a certain
time by means of electric pacemakers; thus we varied the permeabilities and
ionic fluxes electrically. When the driving was stopped, the heart rate
exhibited an undershoot before attaining its spontaneous frequency. The
curves of heart rate were equal to those which reached its new steady state
following a sudden drop of temperature. In the last-mentioned experiments
the permeabilities and ionic concentrations have been simultaneously
varied by means of humoral and ionic factors, as was done in the experi7*
99
factors (driving forces, coefficients and fluxes) in the pacemaker system that
influence the steady state transition of heart rate in capacity adaptation to
temperature? It is well known that heart frequency is a function of the rapidity of diastolic depolarisation of the pacemaker tissues, the rapidity being
a function of the ion diffusion potentials and the specific permeabilities.
According to NERNST'S law, diffusion potentials are dependent on the actual
ion concentration differences in- and outside the cell; they are real steady
state values. Of course, they are dependent on the active and passive ion
transport across the membrane. If the unidirectional passive sodium influx
is greater than the active transport from inside the cell to the intercellular
space, the sodium quotient Nao/Naj is lowered and a decrease of the heart
frequency results; reciprocal conditions hold true for the potassium potential.
The inactivation of acetylcholine at the membrane is increased by temperature more markedly than its rate of replenishment; permeability of
potassium depends on the actual concentration of acetylcholine. The
lowered permeability as a consequence of temperature rise increases the
rapidity of diastolic membrane-depolarization. In the time course of heart
frequency the balance of potassium transport will be shifted toward a
higher rate of active transport; whereas, because of frequent depolarizations, the balance of sodium transport is shifted towards a higher passive
influx rate. Thus, the higher temperature leads to a gradually increasing
potassium potential and a gradually decreasing sodium potential. Following
a rise in temperature, therefore, the heart rate will be lowered starting from
the first maximum-value; it will reach a steady state according to the new
ion transport-balance.
This briefly outlined hypothesis has been tested by experiments with
capacity adaptation after certain variations of permeability and ionic
potentials. This was done by adding to the perfusion medium of the heart
various substances, such as ACh, atropine, eserine, epinephrine and fJreceptor blocking agents. The ionic potentials have been varied by diminishing or increasing the concentration of extracellular sodium or potassium
(or chloride). Under these special circumstances, the steady state transitions
behaved exactly in the mode predicted by our hypothesis.
Finally we carried out another test in order to support the validity of the
hypothesis. At constant temperature the heart rate was doubled for a certain
time by means of electric pacemakers; thus we varied the permeabilities and
ionic fluxes electrically. When the driving was stopped, the heart rate
exhibited an undershoot before attaining its spontaneous frequency. The
curves of heart rate were equal to those which reached its new steady state
following a sudden drop of temperature. In the last-mentioned experiments
the permeabilities and ionic concentrations have been simultaneously
varied by means of humoral and ionic factors, as was done in the experi7*