4. THE CIRCULATORY SYSTEM
153
multiplying stroke volume by the difference between the mean output
and input pressures) increase (Figs. 7 and 8). Increasing input pressures
also cause the rate to increase in the isolated heart. In all probability,
this results from a direct effect of stretch on the pacemaker fibers causing
changes in ionic conductance. Both the increase in rate and stroke
volume contribute to a large increase in cardiac output as the input
pressure is raised.
A rise in temperature increases heart rate both in the isolated preparation and in the intact animal. In the in uitro heart, the rate increases are
offset by decreases in stroke volume as temperature increases, and cardiac
output remains constant. Decreases in temperature, therefore, appear to
have a positive inotropic effect on the heart.
Epinephrine alters the relationship between end diastolic volume and
stroke volume in the isolated trout heart (Figs. 7 and 8). In all cases,
epinephrine increases cardiac output and apparent heart work (calculated by multiplying cardiac output by tht difference between mean
output and input pressures to the heart; in all of these experiments the
heart had to pump saline through a fixed resistance to a height above
the input level). The effect of epinephrine on stroke volume and heart rate
is temperature dependent. At low temperature (SOC), increased epinephrine levels raise heart rate but have little effect on stroke volume (Fig.
7), whereas at high temperatures ( 15OC), stroke volume is increased
but heart rate is decreased (Fig. 8).
In the in uitro trout heart, stroke volume and heart rate are affected
by the input pressure, temperature, and epinephrine. At low temperatures
(SOC), the positive inotropic effect of a decrease in temperature masks
the positive inotropic effect of epinephrine, and only rate increases are observed when epinephrine levels are raised. At high temperatures (15"C),
however, the increased inotropic effect of epinephrine is seen and stroke
volume increases when epinephrine levels are raised. At this temperature
(Fig. 8) the initial rate is high. Systolic emptying is increased so greatly
when epinephrine levels are raised that a longer interval is needed to fill
the heart again. Heart rate appears to be sensitive to stretch of the heart
as well as to temperature and epinephrine; hence, as the heart requires
more time to fill at 15°C when epinephrine levels are increased, the stretch
component determining rate is reduced and heart rate falls (Bennion,
1968). Thus epinephrine exerts both a chronotropic and inotropic effect on
the in uitro trout heart; the positive chronotropic response predominates
at low temperatures, whereas the positive inotropic response predominates at high temperatures. Epinephrine is known to have several
metabolic effects on the mammalian heart. It promotes glycogen breakdown by increasing the level of cyclic AMP, which leads to an increase
153
multiplying stroke volume by the difference between the mean output
and input pressures) increase (Figs. 7 and 8). Increasing input pressures
also cause the rate to increase in the isolated heart. In all probability,
this results from a direct effect of stretch on the pacemaker fibers causing
changes in ionic conductance. Both the increase in rate and stroke
volume contribute to a large increase in cardiac output as the input
pressure is raised.
A rise in temperature increases heart rate both in the isolated preparation and in the intact animal. In the in uitro heart, the rate increases are
offset by decreases in stroke volume as temperature increases, and cardiac
output remains constant. Decreases in temperature, therefore, appear to
have a positive inotropic effect on the heart.
Epinephrine alters the relationship between end diastolic volume and
stroke volume in the isolated trout heart (Figs. 7 and 8). In all cases,
epinephrine increases cardiac output and apparent heart work (calculated by multiplying cardiac output by tht difference between mean
output and input pressures to the heart; in all of these experiments the
heart had to pump saline through a fixed resistance to a height above
the input level). The effect of epinephrine on stroke volume and heart rate
is temperature dependent. At low temperature (SOC), increased epinephrine levels raise heart rate but have little effect on stroke volume (Fig.
7), whereas at high temperatures ( 15OC), stroke volume is increased
but heart rate is decreased (Fig. 8).
In the in uitro trout heart, stroke volume and heart rate are affected
by the input pressure, temperature, and epinephrine. At low temperatures
(SOC), the positive inotropic effect of a decrease in temperature masks
the positive inotropic effect of epinephrine, and only rate increases are observed when epinephrine levels are raised. At high temperatures (15"C),
however, the increased inotropic effect of epinephrine is seen and stroke
volume increases when epinephrine levels are raised. At this temperature
(Fig. 8) the initial rate is high. Systolic emptying is increased so greatly
when epinephrine levels are raised that a longer interval is needed to fill
the heart again. Heart rate appears to be sensitive to stretch of the heart
as well as to temperature and epinephrine; hence, as the heart requires
more time to fill at 15°C when epinephrine levels are increased, the stretch
component determining rate is reduced and heart rate falls (Bennion,
1968). Thus epinephrine exerts both a chronotropic and inotropic effect on
the in uitro trout heart; the positive chronotropic response predominates
at low temperatures, whereas the positive inotropic response predominates at high temperatures. Epinephrine is known to have several
metabolic effects on the mammalian heart. It promotes glycogen breakdown by increasing the level of cyclic AMP, which leads to an increase