First published online March 2, 2006
Journal of Experimental Biology 209, 1024-1034 (2006)
Published by The Company of Biologists 2006
doi: 10.1242/jeb.02082
Temperature dependence of cardiac performance in the lobster Homarus americanus
Mary Kate Worden1,*,
Christine M. Clark1,
Mark Conaway2 and
Syed Aman Qadri1
1 Department of Neuroscience, University of Virginia, PO 801392,
Charlottesville, VA 22908, USA
2 Division of Biostatistics and Epidemiology, University of Virginia, PO
801392, Charlottesville, VA 22908, USA
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Fig. 1. Hourly water temperatures recorded at a lobster trap at a depth of 7
fathoms (12.8 m). Data courtesy of James Manning of the National Oceanographic
and Atmospheric Association and the Environmental Monitors on Lobster Traps
project
(http://www.emolt.org).
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Fig. 2. Temperature of the pericardial sinus increases as external water
temperature warms. The water temperature begins warming from 2°C at time
zero. In this experiment internal and external temperature differed by
1.03±0.14° (mean ± s.e.m.) over the temperature range
2–22°C.
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Fig. 3. Temperature affects the amplitude and frequency of heartbeats recorded from
isolated lobster hearts. Tension recordings of heartbeats at different
temperatures are shown; all are from the same in vitro preparation
and are displayed on the same scale.
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Fig. 4. The strength of the heartbeat depends on temperature. Symbols represent the
estimated mean ratios (±95% confidence intervals) of contraction
amplitudes measured at each temperature relative to those measured at 2°C.
Statistical significance was determined from repeated-measures models using
log scale. Compared to the values at 2°C, contraction amplitudes are
significantly different at temperatures from 12 to 22°C
(P<0.05). For temperatures of 2–16°C, N=9; 18
and 20°C, N=6; 22°C N=5.
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Fig. 5. The rates of contraction and relaxation of the heartbeat depend on
temperature. (A) Tension recordings averaged over 12 successive heartbeats
show the shape of the heartbeat at the indicated temperatures. The inset shows
heartbeats at 2°C and 22°C normalized to the maximal amplitude of the
heartbeat. (B) Phase plots of the rate of change of force (y-axis) as
a function of the force of contraction (x-axis) of the heartbeat.
Plots represent all heartbeats recorded during 1 min at each indicated
temperature. (C) Rates of contraction and of relaxation measured as the mean
(±s.d.) of the maximum rising and falling slopes
(dF/dt) of the heartbeat at indicated temperatures. (D)
Acute Q10 values for the contraction and relaxation of the
heartbeat calculated from the change in dF/dt as a function
of temperature (see Materials and methods). (E) Phase plots of B normalized
for contraction amplitude at each temperature. (F) Rates of contraction and
relaxation from C normalized for contraction amplitude at each temperature.
(G) Acute Q10 values calculated from normalized data in F. All data
are from a single isolated heart.
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Fig. 6. Heart rate depends on temperature. (A) Scatter plots show the frequency of
the heartbeat in isolated hearts (N=10) in vitro as a
function of temperature. Each symbol represents a different heart. The number
of hearts failing at temperatures of 18, 20 and 22°C, was 2, 3 and 5,
respectively. (B) Heart rates from isolated hearts (filled squares) plotted
for comparison with heart rates recorded in intact lobsters in vivo
(filled circles) as a function of temperature. In both data sets there are
significant differences in mean heart rate across temperature
(P<0.0001). Assuming a linear trend, the estimated slopes (means
± s.e.m.) of the lines relating heart rate to temperature in intact
animals and in isolated hearts are 0.040±0.004 and 0.026±0.006,
respectively. *Data are significantly different at P<0.05;
**P<0.001; P-value based on contrast in repeated-measures
model. The P-values are not adjusted for the multiple comparisons.
Even with adjusted differences the data from 12 to 22°C are still
significant.) Only data from beating hearts were included for calculation of
the mean, therefore, for isolated hearts values of N are as follows:
from 2–16°C, N=10; at 18°C, N=8; at 20°C,
N=7; at 22°C, N=5. In intact animals only one heart
failed as temperature increased (at 20°C). Heart rates (means ±
s.e.m.) measured in intact animals in the wild [open symbols; data reproduced
from (Mercaldoallen and Thurberg,
1987 )]. (C) Heart rates in intact animals (N=4) measured
over time as temperature increased from 2°C to a steady state level of
12°C. Horizontal bar indicates time period of temperature change (2 to
12°C) and time period of steady state temperature at 12°C.
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Fig. 7. Values for acute Q10 (means ± s.e.m.) calculated for
heart rates in intact animals and isolated hearts. Values are calculated from
data in Fig. 6B. *Data are
significantly different at P<0.05.
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Fig. 8. Plots showing the relationship between the amplitude of the heartbeat
contraction and the frequency of the heartbeat for seven isolated hearts. Data
were collected as each preparation was warmed from 2 to 22°C. Arrows
indicate direction of warming temperature.
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Fig. 9. Cardiac performance in isolated hearts (N=4) in vitro as
a function of temperature. (A) Examples of blood flow in sternal artery
measured at the indicated temperatures. (B) Heart rate (mean ± s.d.)
measured as a function of temperature. (C) Stroke volume (mean ± s.d.)
measured as a function of temperature. The data show a linear trend with an
estimated slope of –0.070 (s.e.m.=0.017, P<0.001). (D)
Cardiac output (mean ± s.d.), measured as a function of temperature, is
represented by the symbols and solid lines. The broken line represents the
estimated means based on the quadratic equation as follows: mean cardiac
output=19.18(±5.4)+5.01(±0.91)x
(temperature)–0.25(±0.04)x(temperature)2, where
values in parentheses are standard errors. The estimated maximum for the
fitted curve is at temperature=9.90, 95% confidence interval (3.6, 16.2).
*Data are significantly different from values at 2°C
(P<0.05).
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Fig. 10. Serotonin increases the frequency and strength of the heartbeat. (A)
Serotonin increases contraction amplitude to a level that remains at steady
state for more than 10 min at 2°C. (B) Traces show tension recordings at
indicated temperatures under control conditions and after application of
serotonin. All traces in B are from the same isolated heart.
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Fig. 11. Serotonin increases the strength and frequency of the heartbeat in isolated
hearts (N=7). (A) Means of ratios of the amplitude of the contraction
in the presence and absence of serotonin (5-HT) for each preparation are shown
as a function of temperature. There are no statistically significant
differences in amplitude across temperature (P=0.40). (B) Means of
ratios of the frequency of the heartbeat in the presence and absence of
serotonin for each preparation are shown as a function of temperature. There
are no significant differences in heart rate across temperature
(P=0.69). (C) Phase plots for heartbeats recorded in the absence
(control) and presence of serotonin show similar shapes. Each trace shows the
rate of change of force (y-axis) as a function of the force of the
contraction (x-axis) for heartbeats recorded over 1 min at 2°C.
In this experiment serotonin increased contraction amplitude at 2°C by
39.6%.
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© The Company of Biologists Ltd 2006
