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special communication
A new approach to normalize myocardial
temperature in the open-chest pig model
FRANK GRUND,1 HILCHEN T. SOMMERSCHILD,1
KNUT A. KIRKEBØEN,1,2 AND ARNFINN ILEBEKK1
1Institute for Experimental Medical Research, University of Oslo, Ullevål Hospital,
and 2Department of Anesthesia, Ullevål Hospital, 0407 Oslo, Norway
arrhythmia; blood flow; experimental model; infarction; ischemia
account for almost 50% of all
deaths in the Western world (3). Coronary heart disease, i.e., myocardial infarction and sudden death,
accounts for the largest proportion of this mortality.
Much research activity is, therefore, conducted to reveal cardioprotective interventions to reduce cardiovascular mortality. One of the experimental preparations
most often used for this purpose is the open-chest
animal model. This model allows easy access to the
heart for exact measurement of function, metabolism,
and electrophysiological variables and their changes
during various pathophysiological conditions, like regional myocardial ischemia. However, the heart in this
model is exposed to an unphysiological environment.
Exposure to room temperature and evaporation from
the epicardial surface contribute to cardiac cooling.
Because myocardial temperature influences both the
occurrence of arrhythmias (13, 14) and development of
CARDIOVASCULAR DISEASES
2190
necrosis during ischemia (1, 2, 5, 20), it is important to
measure and control this parameter in experimental
settings established to investigate mechanisms of cardiac damage related to ischemia and reperfusion.
Accordingly, much effort has been made to minimize
temperature fluctuations in the open-chest animal
model. One approach is to keep the exposed heart warm
by the use of heating lamps. Heating lamps allow
continuous access to the heart during the experiment.
However, they do not shield the myocardium from
convective air currents and subsequent temperature
fluctuations. To reduce such temperature fluctuations,
the chest with the exposed heart is often covered with
transparent plastic film for insulation. However, insulation prevents easy access to the heart. Therefore, in an
attempt both to reduce temperature fluctuations in the
exposed heart and to maintain easy access to the heart,
we designed and built a thermocage to be placed over
the open thorax.
In the present paper, we present the open-chest pig
model with the thermocage, and we compare data
showing temperature changes, particularly in response
to ischemia, in the anterior left ventricular (LV) wall of
the exposed heart without any thoracic temperaturecontrolling device, after proper positioning of a heating
lamp, and, eventually, after placement of the specially
constructed thermocage. Pigs were used because they
have few native collaterals (23), and, therefore, it was
not necessary to incorporate collateral flow as a covariate in the comparison of temperature changes. Because
both size of ischemic area and depth of myocardial
temperature recordings may influence temperature
changes during ischemia, comparisons of temperature
changes with the heating lamp and the thermocage
were performed on the same pigs. We restricted ischemia to a maximum of 10 min because myocardial
temperature does not, according to pilot studies, change
after this time. Additionally, myocardium subjected to
10 min of ischemia does not develop irreversible cell
injury (16), and repeated recordings can be performed
in the same heart without development of myocardial
infarction.
METHODS
Animal preparation. Animals used in the present study
were maintained and housed in accordance with the condi-
8750-7587/98 $5.00 Copyright r 1998 the American Physiological Society
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Grund, Frank, Hilchen T. Sommerschild, Knut A.
Kirkebøen, and Arnfinn Ilebekk. A new approach to
normalize myocardial temperature in the open-chest pig
model. J. Appl. Physiol. 84(6): 2190–2197, 1998.—To prevent
unphysiological temperature fluctuations in the myocardium
in the open-chest model, we constructed a thermocage. Five
pigs under pentobarbital sodium anesthesia underwent repetitive left anterior descending (LAD) coronary artery occlusions. Myocardial temperature was measured without any
thoracic temperature-controlling device and in the presence
of either a heating lamp or the thermocage. Without any
thoracic temperature-controlling device, the temperature at
5-mm myocardial depth was 1.28 6 0.33°C below the intraabdominal temperature (P , 0.05). During a proximal 5-min
LAD occlusion, myocardial temperature decreased by 1.86 6
1.02°C in the ischemic area (P , 0.05). Both the heating lamp
and the thermocage abolished the difference between intraabdominal and myocardial temperatures and prevented the
decrease in myocardial temperature during ischemia. Only
the thermocage minimized myocardial temperature fluctuations due to air currents and prevented epicardial exsiccation.
We conclude that either a thermocage or a heating lamp may
be used to normalize myocardial temperature in the openchest pig model. However, the thermocage is superior to the
lamp in minimizing temperature fluctuations and preventing
epicardial exsiccation.
MYOCARDIAL TEMPERATURE CONTROL IN OPEN-CHEST MODEL
heating equipment, 2) with the heating lamp, and 3) with the
thermocage placed over the open chest of the pig. In one of the
pigs, equipped with the thermocage, myocardial temperature
measurements were performed at multiple points within the
wall. Room temperature was kept between 22 and 27°C.
In the regions subjected to ischemia, at least one thermocouple was placed to record changes just beneath the epicardial connective tissue, and another was placed ,5 mm deep
into the myocardium. Total coronary occlusion was achieved
either by inflating a hydraulic occluder (within 5 s) or by
application of a Mayfield clip and was verified by a decline in
CBF to zero. Occlusions were only induced during stable CBF.
To reduce accidental air currents during the experiments, all
doors and windows to the operating theater were closed, and
movements of staff members were reduced to a minimum. If
ventricular fibrillation occurred, the heart was given one or, if
necessary, more direct-current countershocks (15–30 J). If
electroconversion was successfully achieved within 1 min, the
animal was allowed to continue the experimental protocol. At
the end of the experiment, the animals were killed by
intracardial KCl injection.
Equipment to control myocardial temperature. To maintain
normal cardiac temperature during ischemia, a 150-W heating lamp (Philips IP 150 R) was used. At intervals, the lamp
was placed 40–45 cm above the heart, so that epicardial
temperature became close to midmyocardial temperature.
The effects of the lamp at that distance were recorded by
several mercury thermometers placed on a table covered with
white cotton sheets. As illustrated in Fig. 1, the central
temperature 45 cm below the lamp, i.e., at the same level as
the heart, was equal to normal temperature for the pig (6),
but the heating effect decreased sharply 5–10 cm away from
the center.
To lessen both convective and evaporative heat loss, the
thermocage was used. Briefly, it consists of double Plexiglas
(,1-cm space between) formed into a top plate and a front and
a back wall (Fig. 2). The space between the Plexiglas was
connected to a heating bath (M3 LAUDA, Dr. R. Wobser; KG,
D-6970 Lauda-Königshofen Postf. 1251, Germany). The two
Fig. 1. Temperatures on a horizontal table covered with white cotton
sheets 45 cm below a heating lamp (150 W). Temperatures recorded
at given radial distances from the center are presented. Maximal
(max) temperature was recorded in central beam underneath center
of the lamp. Room temperature was 24°C.
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tions set by the Norwegian Council for Animal Research. The
investigation conformed with the ‘‘Guide for the Care and Use
of Laboratory Animals’’ [DHEW Publication No. (NIH) 86–23,
revised 1985, Office of Science and Health Reports, DRR/NIH,
Bethesda, MD 20205].
Five domestic pigs of either sex (25.5–33.5 kg) were fasted
overnight and anesthetized with pentobarbital sodium, initially 40 mg/kg body wt ip, followed by a sustaining infusion of
5–20 mg · kg21 · h21 iv pentobarbital sodium, according to the
depth of anesthesia. The pigs were ventilated through a
tracheostoma with 50% oxygen-50% air mixture by using a
volume-regulated ventilator. A positive end-expiratory pressure of 5 cmH2O was established. Ventilation frequency and
volume were adjusted to keep PCO2 and pH within normal
ranges. Polyethylene catheters were placed in the right
femoral vein for administration of drugs and fluids and in the
right femoral artery for blood sampling and pressure recording. The heart was exposed through a midsternal split and
suspended in a pericardial cradle. In two pigs, a 5- to
10-mm-long segment of left anterior descending (LAD) coronary artery, immediately distal to the first major branch, was
dissected free to allow placement of a Mayfield clip for
intermittent occlusions and a transit-time flow probe to
measure coronary blood flow (CBF). Additionally, a 5-mmlong segment distal to the second major branch of LAD was
dissected free to allow intermittent placement of a Mayfield
clip. In three pigs, a 10- to 15-mm-long segment of LAD, distal
to the first major branch, was dissected free to allow placement placement both of a hydraulic occluder and, distal to it,
of a transit time flow probe. Body temperature was maintained at 38.0–39.0°C by using wrappings and a homeothermic blanket system unit (50–7103 Harvard Homeothermic
Blanket System, South Natick, MA), with a thermistor probe
placed in the abdomen. Urine was drained continuously
through a cystostoma. After completion of the surgical preparation, all pigs were allowed a stabilization period of 30 min.
Hemodynamic measurements. A microtip pressure-transducer catheter (Millar Instruments, Houston, TX) was introduced into the LV through the right carotid artery for
measurements of LV pressure and the contractility parameter, the maximal positive value of the first derivative of LV
pressure (LVdP/dtmax ). An electromagnetic flow probe was
placed on the ascending aorta and connected to a squarewave electromagnetic flowmeter (model 376; Nycotron, Drammen, Norway). Arterial blood pressure was measured by a
Statham pressure transducer (model P23 Gb; Gould Instruments, Hato Rey, Puerto Rico). CBF was measured by transittime flowmetry (T208; Transonic Systems).
Hemodynamic variables were continuously recorded on an
eight-channel galvanometric recorder (model 7758 B; HewlettPackard, Medical Products Group, Andover, MA). Immediately before each LAD occlusion, when higher resolution of
data was required, the output of the recorder was sampled at
100 Hz, and the signals were transformed by an analog-todigital converter and stored on floppy disks. Computer samplings of hemodynamic variables were obtained at end expiration, and values from four to six consecutive beats were
averaged by the computer.
Experimental procedure. To evaluate temperature changes
in the anterior LV wall during regional ischemia, all pigs
underwent 8–11 LAD occlusions of 1.5- to 10-min duration. At
least four of these occlusions were of 5-min duration. In two of
the pigs, both proximal and distal LAD occlusions were
performed, in random order, to clarify whether the size of
area at risk influenced myocardial temperature changes
during ischemia. In the remaining three pigs, LAD occlusions
were performed, also in random order, 1) with no thoracic
2191
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MYOCARDIAL TEMPERATURE CONTROL IN OPEN-CHEST MODEL
open sides were closed with wet towels, plastic film, and
finally an insulating coat. Coat sleeves made it possible to
place the hands within the cage without a drop in temperature or humidity. Both a thermometer and a hygrometer (34–
1549 Clas Ohlson, Oslo, Norway) were placed inside the box.
Temperature measurements. To measure temperature
changes, thermocouples, made of insulated constantan and
copper wire (OD 0.075 and 0.09 mm, respectively), soldered
together, and sealed within a polyethylene tube (ID 0.25 mm,
OD 0.75 mm), were inserted into the myocardium and
connected to a reference thermocouple in the pig’s abdomen.
The junction between copper and constantan generates 40
µV/°K. By connecting the constantan part in the myocardium
to the constantan part in the abdomen and connecting the two
copper ends to a recorder, the circuit would generate 40 µV/°C
temperature difference between the two elements. The voltage differences between the cardiac thermocouples and the
reference thermocouple in the pig’s abdomen were therefore
recorded by means of a direct-current amplifier and a sixchannel recorder (Multicorder, model MC6621, Graphtec,
Tokyo, Japan). The actual temperatures recorded by the
thermocouples were obtained by help of a mercury thermometer positioned at the same place as the reference thermocouple. Room temperature and the temperature within the
thermobox were measured with electronic thermometers
(Microprocessor Digital Thermometer, model 819, Tegam,
Geneva, OH). Simultaneous temperature measurements in a
waterbath with all thermometers revealed maximal temperature differences of ,0.25°C for temperatures between 35 and
42°C.
Ischemic area. The size of the ischemic area was estimated
in pigs that underwent both proximal and distal LAD occlusions. After the pigs were killed, 10 ml of 0.1 M sodium
phosphate buffer containing 2% (wt/vol) triphenyltetrazolium
chloride were injected into the LAD at the distal occlusion
site, after the artery just proximal to the injection site had
been tied off. Then, a 10-ml suspension of 2-mg zinc-cadmium
sulfide particles (1–10 µm in diameter; Duke Scientific, Palo
Alto, CA) per milliliter isotonic saline was injected into the
LAD at the proximal occlusion site, after the artery just
RESULTS
Baseline myocardial temperature fluctuations. In the
uncovered open-chest model, we recorded continuous
temperature fluctuations in the myocardium of the LV
wall (Fig. 3). These fluctuations were more pronounced
just beneath the epicardial connective tissue than 5
mm deep into the myocardium and varied between
0.002 and 0.3 Hz. By use of the thermocage, the peak
fluctuation during a 4-min period was reduced to
approximately one-tenth (Table 1) (Fig. 3). Actually,
during shorter time periods, only thermal oscillations
with peak amplitude of ,0.005°C and synchronous
with the ventilation were observed.
Baseline myocardial temperature. In the open-chest
model with no thoracic heating equipment, the temperature just beneath the epicardial connective tissue was
1.89 6 0.55°C below the intra-abdominal temperature
(P , 0.05). At a myocardial depth of 5 mm, it was 0.61 6
0.25°C warmer than at the epicardial surface (P , 0.05)
but still as much as 1.28 6 0.33°C below the intraabdominal temperature (P , 0.05). Both the heating
lamp and the thermocage prevented the difference
between myocardial and intra-abdominal temperatures (Fig. 3).
Figure 4 shows the effect of the thermocage on both
myocardial temperature and temperature fluctuations.
Furthermore, Fig. 4 illustrates that work with one
hand within the thermocage can be performed without
any significant decrease in temperature. When using
the thermocage, which minimized temperature fluctuations due to air currents within the operating theater,
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Fig. 2. Photograph of thermocage that was placed across the open
chest of pigs. Tubings supplied warm water for circulation. Open
sides were closed with wet towels, plastic films, and an insulating
coat (not shown), completely enclosing the open thorax.
proximal to this injection site had been tied off. The heart was
then excised, both atria were removed, and the ventricles
were moulded in 2% agarose at 37°C and cooled in a refrigerator. After the agarose gelled, the ventricles were cut into
,7-mm-thick slices. The slices were cleaned for agarose,
weighed, and placed between two glass slides to a uniform
thickness. The ventricular area, the area distal to the distal
occlusion site (tetrazolium positive), and the area distal to the
proximal occlusion site (tetrazolium positive 1 fluorescent
under ultraviolet light) were traced directly onto acetate
sheets and planimetered on a digitizing tablet (Videoplan 2,
Kontron Electronics, Germany). The weights of the ischemic
areas were then calculated by multiplying the fractions of the
ischemic areas for each slice with the slice weight and
summing the products. Total weight of the ischemic areas was
expressed as a percentage of total ventricular weight. Finally,
the area perfused with triphenyltetrazolium chloride was
carefully examined for any pale regions denoting necrosis.
Statistical analysis. For comparison of hemodynamic data
over time, temperature change over time, and transmyocardial temperature differences, a paired t-test was used. A
one-way repeated-measures ANOVA was used to compare
temperature fluctuations at baseline with no heating equipment, the lamp, and the thermocage. To test the relationship
between hemodynamic variables and myocardial temperature, Pearson product moment correlation coefficient (r) was
calculated. A value of P , 0.05 was considered statistically
significant (two tailed). All values are presented as means 6
SD. Because of continuous fluctuations in myocardial temperature, average values were obtained during 0.5- to 1-min
intervals.
MYOCARDIAL TEMPERATURE CONTROL IN OPEN-CHEST MODEL
2193
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Fig. 3. Recordings showing differences in myocardial and intra-abdominal temperatures (D°C) of exposed heart
when no thoracic heating equipment (A), or when heating lamp (B) or thermocage (C) were used. Temperature
changes by left anterior descending (LAD) coronary artery occlusion in both midmyocardium and epicardium are
shown. Recording pens were separated by 5 mm on the recorder; accordingly, deflections are separated by 20 s, with
paper speed of 15 mm/min for data presentation. Intra-abdominal temperature was set to zero. Both heating lamp
and thermocage prevent cardiac cooling, but only thermocage reduces fluctuations in myocardium to a minimum.
we found that myocardial temperature in the midwall
was 0.37 6 0.05°C higher than that of LV cavity blood.
Myocardial temperature during ischemia. When no
thoracic heating equipment was used during a 5-min
LAD occlusion, myocardial temperature decreased significantly in the ischemic region (Fig. 3). Just beneath
the epicardial connective tissue, the temperature decreased by 2.10 6 1.01°C (P , 0.05) and at 5-mm depth
by 1.86 6 1.02°C (P , 0.05). Both the heating lamp and
the thermocage prevented this decrease in temperature
(Fig. 3). Actually, the thermocage enabled us to observe
a reproducible temperature increase during each of the
2194
MYOCARDIAL TEMPERATURE CONTROL IN OPEN-CHEST MODEL
Table 1. Baseline fluctuations in myocardial
temperature
Myocardial Temperature, °C
Myocardial Depth, mm
Control
Lamp
Thermocage
1
5
0.63 6 0.20
0.28 6 0.03
0.55 6 0.06
0.28 6 0.07
0.05 6 0.02*
0.03 6 0.02*
Baseline-temperature fluctuations (means 6 SD) were defined as
peak amplitude during 4 min at stable coronary blood flow. * P , 0.05
vs. both control and lamp.
Fig. 4. Myocardial temperature changes
when a hand is put into thermocage
and when thermocage is removed and
replaced. Intra-abdominal temperature was set to zero.
DISCUSSION
The present study demonstrates that cardiac cooling,
both at baseline and during LAD occlusions in the
open-chest pig model, can be avoided by the use of
either a heating lamp or a thermocage. However, only
the thermocage prevents epicardial exsiccation and
reduces fluctuations in myocardial temperature to a
minimum.
In an experimental model, designed to find potential
cardioprotective interventions against ischemia and
reperfusion damage, one should ideally control all
factors that might influence myocardial damage. In the
open-chest animal model, determinants of infarct size,
such as duration of ischemia, the size of area at risk,
collateral blood flow, and myocardial oxygen demand
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LAD occlusions for the first 60 6 9 s of ischemia,
amounting to between 0.04 and 0.16°C, depending on
the position of the thermoelement. This increase in
temperature occurred both when the temperature
within the thermocage was 0.5°C above and when it
was 0.5°C below the intra-abdominal temperature.
Sometimes a slight increase in myocardial temperature
was also noticed during ischemia when the heating
lamp was used. However, due to the large temperature
fluctuations in the uncovered myocardium, precise
temperature measurements were difficult to obtain.
In the two pigs in which the size of the ischemic area
was varied, proximal LAD occlusions induced a larger
decline in temperature, measured centrally in the
ischemic area that constituted 18 6 8% of the ventricular weight, than did distal LAD occlusions that caused
ischemia in only 5 6 3% of the ventricular weight. This
observation is presented in Fig. 5. The decline in
temperature by repeated distal or by repeated proximal
LAD occlusions was highly reproducible within each
animal. No sign of necrosis was found in the area that
was subjected to ischemia by both proximal and distal
LAD occlusions.
Epicardial exsiccation. In the uncovered open-chest
model, there was a visible exsiccation of the epicardial
surface during ischemia. Epicardial exsiccation, identified as a dry surface with poor reflection of light, was
especially pronounced when the heating lamp was used
to maintain myocardial temperature during ischemia.
The thermocage prevented epicardial exsiccation during ischemia, as a relative humidity .90% was easily
obtained within the cage.
CBF and myocardial temperature. Blood gases and
hemodynamic variables recorded at start and end of the
experimental procedure, lasting on average 5 h 42
min 6 2 h 42 min, are presented in Table 2. Whereas
the blood gases were kept stable by respiratory adjustment, LV systolic pressure fell by 22 6 16 mmHg (P ,
0.05), LVdP/dtmax by 26 6 18% (P , 0.05), aortic flow by
27 6 16% (P , 0.05), and CBF by 29 6 12% (P , 0.05).
No significant changes were found in heart rate and
mean arterial pressure.
In all experiments, CBF decreased slowly in the
course of the experimental protocol. When no thoracic
heating equipment was used, the decrease in CBF was
accompanied by an increased difference between the
intra-abdominal and myocardial temperatures. Accordingly, a significant correlation was found between CBF
and the difference between myocardial and intraabdominal temperatures. Data from one experiment
are shown in Fig. 6. The influence of CBF on myocardial
temperature was also detected during reactive hyperemia with no thoracic heating equipment, when myocardial temperature approached the intra-abdominal temperature (Fig. 3). With the thermocage applied,
midmyocardial temperature, on the contrary, declined
during postischemic hyperemia (Fig. 3). No significant
correlation was found between the rate-pressure product (heart rate multiplied by mean arterial pressure)
and the difference between myocardial and intraabdominal temperatures.
MYOCARDIAL TEMPERATURE CONTROL IN OPEN-CHEST MODEL
2195
Fig. 5. Myocardial temperature changes
by a distal (A) and a proximal (B) LAD
occlusion in open-chest pig model without any thoracic heating equipment.
Intra-abdominal temperature was set
to zero. Both epicardial and midmyocardial recordings were obtained. Epicardial temperature was lower than midmyocardial temperature.
dial temperature (7); myocardial temperature gradients may induce dispersion of refractoriness and,
thereby, the occurrence of artificial arrhythmias. Furthermore, transmyocardial temperature gradients in
the open-chest model may result in small epi/endo
infarct size ratios and, thereby, lead to erroneous
conclusions about how infarction actually evolves in the
intact organism. The influence of temperature on infarction in the open-chest pig model has been studied by
Duncker et al. (2). These reasearchers occluded the
LAD for 45 min at different temperatures and found, by
linear regression analysis, that 20% of the area at risk
Table 2. Blood gases and hemodynamic variables at
start and end of the experimental procedure
Variable
Start
End
Arterial PO2 , kPa
Arterial PCO2 , kPa
Arterial pH
HR, beats/min
MAP, mmHg
LVSP, mmHg
LVdP/dtmax , mmHg/s
AF, l/min
CBF, ml/min
30.6 6 1.9
6.0 6 0.6
7.40 6 0.04
108 6 10
102 6 16
129 6 14
3,222 6 507
2.89 6 0.83
18 6 2
30.7 6 4.8
5.5 6 0.8
7.40 6 0.01
117 6 15
86 6 7
106 6 14*
2,324 6 341*
2.14 6 0.88*
12 6 1*
Values are means 6 SD of 5 pigs. HR, heart rate; MAP, mean
arterial pressure; LVSP, peak left ventricular systolic pressure;
LVdP/dtmax , maximal positive value of 1st derivative of left ventricular pressure; AF, aortic flow; CBF, coronary blood flow. * P , 0.05 vs.
start value.
Fig. 6. Coronary blood flow (CBF) as %flow at start of experiment,
plotted against difference between intra-abdominal and myocardial
temperatures (D°C) in open-chest pig model without any thoracic
heating equipment. Data were obtained immediately before each
occlusion in 1 pig. Note both lower temperature and larger variation
just beneath epicardial connective tissue (r) than at 5-mm myocardial depth (s). CBF correlates with myocardial temperature, both at
epicardial surface and at 5-mm depth (r 5 0.80 and 0.94, respectively;
P , 0.05 for both). Regression lines for both depths are shown.
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are well known (8, 10, 11, 15, 17–19). However, only
recently have myocardial temperature variations in the
normothermic range been shown to greately influence
infarct size development. In the open-chest pig model,
we found a significant difference between the epicardial
and intra-abdominal temperatures, when no thoracic
heating equipment was used, both at baseline and
during ischemia. The magnitude of this difference
showed a large variability, both within pigs and between pigs, depending on the position of the myocardial
thermocouples, CBF, and the size of the ischemic area.
Our study emphasizes the importance of measuring
and controlling temperature in the myocardium and
not relying only on rectal temperature. As myocardial
temperature influences both occurrence of arrhythmias
(13, 14) and development of necrosis during ischemia
(1, 2, 5, 20), this aspect is most important in studies
designed to reveal cardioprotective mechanisms against
ischemia and reperfusion damage.
When transmyocardial temperature gradients, as
observed in the present study, are not taken into
consideration, both misleading and confusing conclusions may be drawn. With regard to arrhythmias,
duration of cardiac action potentials depends on myocar-
2196
MYOCARDIAL TEMPERATURE CONTROL IN OPEN-CHEST MODEL
and repeated recordings can be performed in the same
heart without development of myocardial infarction.
Examination of epicardial exsiccation was only determined by visual inspection. Accordingly, we did not
further quantify the extent of epicardial exsiccation.
However, this might be necessary when studies are
performed to examine physiological consequences of
epicardial exsiccation in the open-chest model.
In conclusion, to control myocardial temperature
fluctuations and avoid transmyocardial temperature
gradients in the open-chest pig model, either a thermocage or a heating lamp may be used. Both the thermocage and the lamp allow continuous inspection and
manipulation of the heart, but only the thermocage
prevents epicardial exsiccation and almost completely
prevents all unphysiological temperature fluctuations.
The authors are grateful for the skilled technical assistance
offered by Gerd Torgersen and Turid Verpe. Special thanks to Severin
Leraand for making the thermocouples and to Bjørn Amundsen for
building the thermocage.
This study was supported by the Norwegian Council on Cardiovascular Diseases, by Prof. Carl Semb’s Medical Research Fund, and by
Anders Jahre’s Fund for the Promotion of Science.
Address for reprint requests: F. Grund, Institute for Experimental
Medical Research, University of Oslo, Ullevål Hospital, 0407 Oslo,
Norway (E-mail: [email protected]).
Received 13 November 1997; accepted in final form 17 February
1998.
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became infarcted for each 1°C increase in body core
temperature.
By using both the heating lamp and the thermocage,
we were able to simulate the closed-chest situation
with regard to temperature, with an intrathoracic
temperature close to rectal temperature (21). The heating lamp resulted, however, in a significant epicardial
exsiccation during ischemia, an unphysiological side
effect with unknown effects. Furthermore, correct use
of the heating lamp required measurement of temperature within the epicardium. The thermocage secured a
stable cardiac environment with regard to both temperature and humidity. Thus evaporative heat loss was
almost completly avoided. Furthermore, it minimized
myocardial temperature fluctuations and thereby allowed precise temperature recordings. As the waterheated side and top panels prevented condensation,
continuous inspection of the heart was possible. Inspection is often necessary when manipulation on the heart
is performed or when easy verification of ischemia
should be obtained. Both the heating lamp and the
thermocage allowed manipulation of the heart without
significant changes in myocardial temperature.
Methodological consideration. By using a paired design, it was unnecessary to incorporate both size of
ischemic area and position of thermoelements as covariates when comparing temperature changes during the
three different interventions. Furthermore, the experimental design enabled us to detect significant differences by use of only a few animals. The use of pigs, with
few native collaterals, secured an almost identical
degree of ischemia during repetitive occlusions. Therefore, temperature differences due to collateral flow
were avoided. Due to the paired design, it was possible
to keep the animal preparation essentially stable during the experimental protocol. The homeothermic heating system allowed us to keep the intra-abdominal
temperature within a narrow range. However, we recorded a decrease in LV systolic pressure, LVdP/dtmax,
aortic flow, and CBF during the experiment. The decrease in CBF, probably representing an adjustment to
both a decreased energy demand in stunned myocardium (4, 12) and a decreased global cardiac work
requirement, influenced the myocardial temperature
during periods with no thoracic heating equipment. To
compensate for the hemodynamic changes, the different interventions were performed in random order, and
only the median value from each intervention was used.
It is well known that both the occurrence of ventricular fibrillation and the duration of reactive hyperemia
increase with increasing occlusion time (9, 22). Accordingly, to limit the occurrence of ventricular fibrillation
and to reduce the total duration of experiments, the
reproducibility of temperature changes induced by
ischemia was mainly evaluated by short occlusion
periods. However, to confirm stable myocardial temperature during ischemia with the heating equipment,
longer lasting occlusions were also performed. The
longer lasting occlusions were restricted to a maximum
of 10 min, because myocardium subjected to 10 min of
ischemia does not develop irreversible cell injury (16),
MYOCARDIAL TEMPERATURE CONTROL IN OPEN-CHEST MODEL
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