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Division of Cardiology, Department of Medicine and Department of Biomedical Engineering, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21287
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The conductance catheter method has
substantially enhanced the characterization of in vivo cardiovascular
function in mice. Absolute volume determination requires assessment of
parallel conductance (Vp) offset because of
conductivity of structures external to the blood pool. Although such a
determination is achievable by hypertonic saline bolus injection, this
method poses potential risks to mice because of volume loading and/or
contractility changes. We tested another method based on differences
between blood and muscle conductances at various catheter excitation
frequencies (20 vs. 2 kHz) in 33 open-chest mice. The ratio of mean
frequency-dependent signal difference to Vp
derived by hypertonic saline injection was consistent [0.095 ± 0.01 (SD), n = 11], and both methods were strongly
correlated (r2 = 0.97, P < 0.0001). This correlation persisted when the ratio was prospectively
applied to a separate group of animals (n = 12), with a
combined regression relation of Vp(DF) = 1.1 * Vp(Sal) 
2.5 [where
Vp(DF) is Vp derived by
the dual-frequency method and Vp(Sal) is
Vp derived by hypertonic saline bolus
injection], r2 = 0.95, standard error of
the estimate = 1.1 µl, and mean difference = 0.6 ± 1.4 µl. Varying Vp(Sal) in a given animal
resulted in parallel changes in Vp(DF) (multiple
regression r2 = 0.92, P < 0.00001). The dominant source of Vp in mice was
found to be the left ventricular wall itself, since surrounding the heart in the chest with physiological saline or markedly varying right
ventricular volumes had a minimal effect on the left ventricular volume
signal. On the basis of Vp and flow
probe-derived cardiac output, end-diastolic volume and ejection
fraction in normal mice were 28 ± 3 µl and 81 ± 6%,
respectively, at a heart rate of 622 ± 28 min
1.
Thus the dual-frequency method and independent flow signal can be used
to provide absolute volumes in mice.
mouse; hemodynamics; ventricular function; methods
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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THE RECENT ADAPTATION of a conductance-micromanometer catheter to the mouse heart has provided a valuable new tool for assessing in vivo cardiovascular performance in normal and genetically modified animals (7, 9, 15). The catheter is composed of two pairs of electrodes with an intervening pressure sensor and is placed along the longitudinal axis of the left ventricular (LV) chamber. A high-frequency low-amperage current is injected between base and apical electrodes, and the measured voltage between the pair of intervening electrodes provides a signal inversely proportional to conductance and, hence, cavity blood volume. First developed for larger mammalian (2, 3, 13) and human hearts (4, 17), the method has been recently applied to hearts of smaller species, including rabbit (1), rat (12, 18), and mouse (9).
Initial validation studies of the conductance catheter in mice were performed by calibrating the signal amplitude to the stroke volume derived by aortic flow probe (9). This provided absolute stroke volume, but not absolute LV volume. Although many indexes of ventricular function can be determined from calibrated relative volume changes, the addition of absolute calibration is important for determining ejection fraction and assessing chamber remodeling, which often plays an important role in disease conditions.
Absolute volume calibration requires estimation of a signal offset (parallel conductance, Vp) due to extension of the current field beyond the LV blood pool into the myocardium and surrounding structures. Vp can be estimated by injecting a small bolus of hypertonic saline (4, 24) to selectively vary the conductivity of cavity blood. A fundamental assumption of this method is that underlying hemodynamics are unchanged by the hypertonic saline bolus. However, the bolus can present a salt load and induce a negative inotropic response. These limitations may become problematic in mice, particularly those with genetically engineered models of cardiac dysfunction, given the small circulating blood volume of only ~2 ml (5).
An alternative method, first reported by Gawne et al. (8) in adult swine, exploits differences between blood and muscle conductivity as a function of varying excitation frequencies. It is well established that blood has a constant conductivity over the range of frequencies from 2 to 100 kHz (19), whereas muscle is more conductive at frequencies >12 kHz (21, 26). Gawne et al. reported that the difference in conductance catheter signal with 3.3- vs. 33-kHz excitation was directly correlated with Vp estimated by hypertonic saline. The goal of the present study was to test the validity of the dual-frequency method for Vp assessment in mice. As a secondary goal, we explored the sources of Vp in the mouse specifically associated with the use of a single-segment conductance system. Our data support the utility of the dual-frequency approach and show that Vp is minimally influenced by conductance from structures outside the LV wall itself (i.e., far-field effects) in mice.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Theoretical formulation.
In accordance with Gawne et al. (8), the differences in
volume signal from varying excitation frequency should be related to
Vp estimated by hypertonic saline bolus by a
proportionality constant
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(1) |
is the average change
in volume signal over the cardiac cycle with use of 2- vs. 20-kHz
excitation frequencies, Vp is the parallel
conductance determined by the hypertonic saline injection method, and
is an experimentally derived constant. If one applies an
instrumentation amplifier gain (a) and offset (b)
to the output signal of the conductance catheter system,
Vp will be influenced by both factors, whereas
will be sensitive solely to the
gain. However, Eq. 1 can be reformulated to include an
amplifier gain a and offset b
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(2) |
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· cm). Results are displayed in Fig. 1C. When considered over a very broad volume range spanning near zero to
five times normal heart size, the volume-conductance signal relationship was nonlinear, as predicted by theory (21).
However, this relationship was very linear within the normal operating range of the mouse heart (<40 µl), confirming recent data
(24), and also linear but with a lower slope at much
higher volumes. Importantly, in the absence of a parallel conductance,
these relationships were virtually identical regardless of the
stimulation frequency.
In vivo study protocol. In vivo studies were performed in accordance with the guidelines of the Animal Care and Use Committee of The Johns Hopkins University. Mice (n = 33) composed of FVB, Black Swiss, C57BL/6, and 129/SV strains 3-12 mo of age were studied. Induction of anesthesia was achieved by placing the animal in a jar containing gauze soaked with methoxyflurane (Schering-Plough Animal Health, Union, NJ) and then intraperitoneally injecting the animal with urethan (750-1,000 mg/kg), etomidate (5-10 mg/kg), and morphine (1-2 mg/kg). A tracheostomy was performed, and a blunt 19-gauge needle was inserted into the trachea. The animal was then connected to a custom-designed, constant-flow mouse ventilator with tidal volume set to 6.7 µl/g at 140 breaths/min. The left external jugular vein was exposed by blunt dissection and cannulated with a 30-gauge needle. Fluid supplementation (100 µl saline or 12.5% human albumin) was provided at 50 µl/min. The LV apex was exposed via a subdiaphragmatic incision, leaving the chest wall and sternum largely intact. The pericardium was opened at the apex, and an apical stab was made with a 26-gauge needle to place a 1.4-F, four-electrode pressure-volume catheter (model SPR-719, Millar Instruments) along the long axis. The pressure-volume catheter was connected to a custom-designed conductance system producing a constant current of 30 µA at a frequency of 2 or 20 kHz. Correct catheter positioning was confirmed by on-line visualization of the pressure-volume loops and placement of the distal electrode within the chamber.
After stabilization, steady-state data were recorded for 3 s (typically 25-30 successive cardiac cycles) at 2 and 20 kHz in random order. At 20 kHz, a 10- to 20-µl bolus of 30% saline was rapidly injected into the left jugular vein to yield an estimate of Vp. From in vitro measurements, it was determined that ~5 µl of the total injected volume contributed to the saline dilution, whereas the remainder resulted from inertial flow due to pressure buildup in the high-resistance tubing during the rapid injection. The latter discharged much too gradually to contribute to abrupt blood conductivity changes. In most studies, one saline injection was performed. In 10 studies, we performed three sequential injections to assess the impact on volume loading and contractility and to test correlations between the two Vp estimation methods in the same animal. All measurements were made with ventilation temporarily suspended at end expiration. Aortic flow was also measured in a subset of 11 normal mice. Animals were placed on their left side, and a small thoracotomy was made between intercostal spaces 5-8 for insertion of an ultrasound perivascular flow probe (model 1RB, Transonics, Ithaca, NY) around the midthoracic aorta. Integration of aortic flow per beat yielded stroke volume, which was used to calibrate stroke volume by conductance catheter. Data were digitized at 2 kHz and analyzed using custom-developed software.Data analysis and protocols.
Vp by the hypertonic saline injection method was
determined by the method of Baan et al. (4), as modified
by Lankford et al. (14). This approach provides multiple
Vp estimates spanning the time from maximal to
minimal first derivative of LV pressure (dP/dt) and computes
a mean value from the estimates. Full details of the method
and computer code for its implementation have been published
(14). was computed as
follows. Volume waveforms from 5-10 sequential cardiac cycles at 2 or 20 kHz were temporally averaged and then digitally resampled to
yield 100 equally time-spaced values (heart rate was identical for
both). The signals were then subtracted from one another to yield a
mean difference curve, and the average difference was
.
during the
full cardiac cycle was assessed in 10 mice. These animals comprised a
group of wild-type and mutant mice, the latter bearing a point mutation in the troponin T gene (16). In a separate group
of 11 animals, we determined and
Vp and determined the ratio of to Vp ( in
Eqs. 1 and 2). Cardiac output was determined independently by aortic flow probe, allowing unit conversion to microliters. A third group of 12 mice was used to further validate the
dual-frequency method, employing the value derived from the second
group of animals. For this test group, we purposely altered the
instrumentation amplifier gain and offset settings to fully test the
general formula in Eq. 2. This group was also used to study
effects of three hypertonic saline injections and compare changes in
Vp by both methods in the same animal. Values are means ± SD.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Temporal variation of LV volume due to altered excitation
frequency.
Figure 2A displays the effect
of altering catheter excitation-frequency in an in vivo mouse heart.
The catheter signal was always greater at 20 kHz, consistent with the
anticipated increase in myocardial conductivity at higher frequency. No
nonlinearity or phase difference was introduced in the volume signal by
switching between 2 and 20 kHz (Fig. 2B). The absolute
difference between the two waveforms was not constant but declined
slightly during systolic ejection (Fig. 2C). However, as
demonstrated in this example, this cyclic variation was typically <1
µl and compatible with shape influences on the conductance signal
(20) or slight changes in myocardial resistivity
(21) during systole. Summary data from 10 mice confirming
this small but consistent variability are shown in Fig. 2D.
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throughout the cardiac cycle.
In vivo study and calculation of .
Figure 3, A and B,
shows recordings for Vp determination by
hypertonic saline injection. Despite saline injection, the change in
peak dP/dt (A) was negligible, indicating that
chamber load and contractility were unaltered by the maneuver. Figure
3B shows calculation of Vp by the
method of Lankford et al. (14). During the saline
wash-in phase, each cardiac cycle was divided into 20 equally
time-spaced intervals spanning maximum to minimum dP/dt, and these values were plotted as the ordinate. Conductivity for each
beat was calculated relative to baseline (from proportional increase in
apparent stroke volume) and plotted on the abscissa. For each
isochrone, regression of volumes vs. relative conductance yielded a
Vp, and the average of these values was
determined. Figure 3, C and D, shows
corresponding uncalibrated volume-time and pressure-volume data at 2- and 20-kHz excitation. The mean difference in volume curves or
was 18.2 AU, yielding a ratio
= 0.102. Similar analyses were performed in 11 animals to
derive a mean value of = 0.095 ± 0.0075 (coefficient of
variation = 7.7%).
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1 (cardiac output ~12.5 ml/min). When the amplitude
of the conductance signal at 20 kHz was matched to this stroke volume,
the stroke volume assessed at the lower frequency was not significantly
changed (19.9 ± 2.7 µl, P = NS). Volume data
were fully calibrated on the basis of the stroke volume and
Vp measurements. The resulting end-diastolic
volume was 28 ± 3 µl and ejection fraction was 81 ± 6%
in these normal mice, consistent with recent noninvasive data
(21, 24). Maximal dP/dt was
17,355 ± 1,540 mmHg/s in these animals.
Validation study.
To further verify Eq. 2, studies were performed in a
separate group of 12 animals, including 4 animals harboring a point
mutation in the 
-myosin heavy chain gene (9). The
instrumentation amplifier gain and offset were purposely changed to
yield new values for a and b (a = 0.32 AU/µmho, and b = 181 AU). The resulting
values of Vp averaged 454.5 ± 33.9 and 463.1 ± 38.4 AU derived by Eq. 2 on the basis
of dual-frequency data. The mean difference was 8.6 ± 21.2 AU,
which translated to ~0.6 ± 1.4 µl on the basis of relations
between arbitrary units and microliters determined from the
simultaneous flow probe/catheter studies. Thus calibration of absolute
volume by the dual-frequency method yielded results to within 1-2
µl of that determined by saline dilution.
3.98 (r2 = 0.97, P < 0.00001, SE of the estimate = 1.1 µl), where
Vp(DF) is Vp determined
by the dual-frequency method and Vp(Sal) is
Vp determined by hypertonic saline bolus
injection. Because the hypertonic saline method itself contained some
variability, we performed Bland-Altman analysis (Fig. 4B).
As evidenced by the small mean difference between the two methods (0.21 µl), there was no bias introduced by the dual-frequency method. The
standard deviation of the mean difference (1.202) was significantly
smaller than the standard deviation of either method
[Vp(Sal) = 5.1 and
Vp(DF) = 4.5], indicating that the two
methods were directly correlated.
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Sources of parallel conductance in the mouse.
In larger mammals, Vp has been shown to stem
from the myocardial wall as well as structures extending beyond the
cavity, such as the right ventricular (RV) blood pool and thorax.
However, the concordance of saline calibration and dual-frequency
methods in the mouse suggested that the physiological determinants of Vp in this setting might stem principally from
the myocardial wall alone. This is because conductivity of RV blood and
thoracic structures would not be expected to vary with frequency and,
thus, would not be well differentiated by the latter method. To further test this hypothesis, we markedly altered the conductivity surrounding the heart by flooding the chest with warm physiological saline. Figure
5 displays representative traces showing
remarkable constancy of the LV volume signal and pressure-volume loop,
despite this intervention. To test the role of RV blood volume, we
compared end-systolic pressure-volume relationships derived by
occlusion of the inferior vena cava (RV volume depletion) or rapid
inflation of the lung (obstruction to pulmonary artery outflow, i.e.,
RV volume expansion). The latter maneuver was previously reported to
generate a steeper rightward-shifted end-systolic pressure-volume relationship than the former maneuver in intact dogs (11).
However, in the mouse, both sets of relations could be superimposed
(Fig. 6).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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This study demonstrates that the dual-frequency excitation method provides a reliable method for estimating the parallel conductance offset of the conductance catheter in mice, extending earlier data of Gawne et al. (8), who first reported on this method in swine. On average, we found Vp to be 10.5 times the magnitude of the signal shift induced by varying excitation frequency at 2 vs. 20 kHz. This ratio was generated in one group of animals and then verified in a second separate group. The second major finding in this study is that the parallel conductance of the mouse heart studied with the present catheter configuration is largely attributable to near-field (i.e., LV wall) effects. This greatly enhances the stability of the signal and simplifies the process of calibration.
In contrast to the present results and those of Gawne et al.
(8), White et al. (23) found a poor
correlation between Vp and the
dual-frequency-derived estimate in adult and neonatal swine.
Interestingly, these authors did not observe significant changes in
stroke volume as a function of frequency within the range employed in
the present study, so this could not explain the discrepancy. However,
conductances were first converted to volumes, by measuring blood
resistivity and cardiac output (independent flow measurement), before
the calculation of . This may have introduced variance into the
estimates, unless the system was also very carefully adjusted so that
zero-input conductance translated to zero-output volts (e.g., Eq. 2). In our study, we applied an identical gain and offset to all
signals, as required by Eq. 1, before determining ,
making ratios comparable between animals. Once calculated, this value
of could be easily applied to other gain and offset settings (i.e.,
Eq. 2), as we tested in the validation group.
One of the more striking findings in this study was the limited
influence of conductance changes outside the LV myocardium on the
volume catheter signal. This is in marked contrast to studies performed
in larger animals in which simply placing a conducting forceps on the
wall distorts the signal (6) and increasing blood volume
within the RV or pericardium greatly increases the parallel conductance
offset (13). In the mouse, filling the chest with saline
or greatly expanding RV blood volume had a minimal effect. However,
particular features of the murine catheter may explain these findings.
The mouse system employs a single sense segment that is placed close to
the stimulating electrodes (<0.5 mm). Previous studies showed that
this arrangement favors near-field contributions, reducing effects of
conductances farther from the sense electrodes (20). The
mouse heart is also relatively thick, with a wall thickness-to-cavity
radius ratio of ~1.0 in normal hearts (25). This may
further contribute to lowering far-field effects. The value of
Vp obtained in the present and recent studies (24) averaging 20-30 µl is consistent with the
~100-mg wall mass of the murine heart and reduced conductivity of
myocardium (about one-third that of blood). When sense and current
electrodes are in very close proximity and certainly when they are
identical, lead impedance can contribute to the offset. However, this
effect was minimized in our system by using a high-input-impedance
amplifier (2 M) for the sense electrodes.
Although the present study verified a simple alternative to saline calibration, the latter method can certainly be used in mice. The potential disadvantages relate to cardiodepression from the hypertonic solution and effects of volume loading. One might reduce these problems by using less-concentrated solutions (i.e., 10-20%); however, we found that this necessitated even more rapid injections to preserve adequate signal-to-noise ratio for analysis, and this was often difficult to achieve. Furthermore, Herrera et al. (11) reported that 30% saline at 40°C was the optimal injectate by yielding the least variability in Vp estimates. Efforts to reduce injectate volume were limited by the requirement for small catheters with high resistance while rapid bolus delivery was required. The dual-frequency approach simplifies this process and provides a method that does not require intravenous fluid administration. This may be a particular advantage, inasmuch as attempts are made to translate this methodology to chronically instrumented animals.
There are some limitations to our analysis. We did not attempt to determine absolute in situ cardiac volumes based on an imaging method (i.e., magnetic resonance or echocardiographic images) to further verify the Vp measurements. Preliminary studies revealed that the catheter itself induced major artifacts in both types of images, and thus the analysis could not be performed simultaneously. Furthermore, our primary aim was to test the similarity between the saline-calibration and dual-frequency methods. The former has been validated in a variety of systems in which simultaneous direct volume measurements are feasible (4). An important caveat to the dual-frequency method was the need to ensure placement of the apical electrode within the blood pool and not the myocardium, as the latter yielded an underestimation of the shift in volume signal due to frequency.
Conclusion. With the ability to estimate absolute volume and the enhanced stability of the signal as a result of near-field effects, the conductance catheter provides a very powerful technique to assess cardiovascular function in the mouse. The dual-frequency method is advantageous, as it can be applied to any conductance system, avoids potential complications of hypertonic saline injections, and allows for estimates to be made repeatedly during a given study. Furthermore, this method can be implemented in real time by employing dual-excitation and filtering electronics, making continuous calibrated volume signals feasible.
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FOOTNOTES |
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Address for reprint requests and other correspondence: D. A. Kass, Halsted 500, The Johns Hopkins Medical Institutions, 600 N. Wolfe St., Baltimore, MD 21287 (E-mail: dkass{at}bme.jhu.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Received 13 August 1999; accepted in final form 12 January 2000.
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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R. J. Hassink, K. B. Pasumarthi, H. Nakajima, M. Rubart, M. H. Soonpaa, A. B. de la Riviere, P. A. Doevendans, and L. J. Field Cardiomyocyte cell cycle activation improves cardiac function after myocardial infarction Cardiovasc Res, April 1, 2008; 78(1): 18 - 25. [Abstract] [Full Text] [PDF]
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K.A. Connelly, D.J. Kelly, Y. Zhang, D.L. Prior, J. Martin, A.J. Cox, K. Thai, M.P. Feneley, J. Tsoporis, K.E. White, et al. Functional, structural and molecular aspects of diastolic heart failure in the diabetic (mRen-2)27 rat Cardiovasc Res, November 1, 2007; 76(2): 280 - 291. [Abstract] [Full Text] [PDF]
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J. M. Nielsen, S. B. Kristiansen, S. Ringgaard, T. T. Nielsen, A. Flyvbjerg, A. N. Redington, and H. E. Botker Left ventricular volume measurement in mice by conductance catheter: evaluation and optimization of calibration Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H534 - H540. [Abstract] [Full Text] [PDF]
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K. C. Bilchick, J. G. Duncan, R. Ravi, E. Takimoto, H. C. Champion, W. D. Gao, L. B. Stull, D. A. Kass, and A. M. Murphy Heart failure-associated alterations in troponin I phosphorylation impair ventricular relaxation-afterload and force-frequency responses and systolic function Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H318 - H325. [Abstract] [Full Text] [PDF]
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M. Reyes, M. E. Steinhelper, J. A. Alvarez, D. Escobedo, J. Pearce, J. W. Valvano, B. H. Pollock, C.-L. Wei, A. Kottam, D. Altman, et al. Impact of physiological variables and genetic background on myocardial frequency-resistivity relations in the intact beating murine heart Am J Physiol Heart Circ Physiol, October 1, 2006; 291(4): H1659 - H1669. [Abstract] [Full Text] [PDF]
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K. A. Connelly, D. L. Prior, D. J. Kelly, M. P. Feneley, H. Krum, and R. E. Gilbert Load-sensitive measures may overestimate global systolic function in the presence of left ventricular hypertrophy: a comparison with load-insensitive measures Am J Physiol Heart Circ Physiol, April 1, 2006; 290(4): H1699 - H1705. [Abstract] [Full Text] [PDF]
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T. E. Claessens, D. Georgakopoulos, M. Afanasyeva, S. J. Vermeersch, H. D. Millar, N. Stergiopulos, N. Westerhof, P. R. Verdonck, and P. Segers Nonlinear isochrones in murine left ventricular pressure-volume loops: how well does the time-varying elastance concept hold? Am J Physiol Heart Circ Physiol, April 1, 2006; 290(4): H1474 - H1483. [Abstract] [Full Text] [PDF]
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K. Uemura, T. Kawada, M. Sugimachi, C. Zheng, K. Kashihara, T. Sato, and K. Sunagawa A self-calibrating telemetry system for measurement of ventricular pressure-volume relations in conscious, freely moving rats Am J Physiol Heart Circ Physiol, December 1, 2004; 287(6): H2906 - H2913. [Abstract] [Full Text] [PDF]
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D. G. Soergel, D. Georgakopoulos, L. B. Stull, D. A. Kass, and A. M. Murphy Augmented systolic response to the calcium sensitizer EMD-57033 in a transgenic model with troponin I truncation Am J Physiol Heart Circ Physiol, May 1, 2004; 286(5): H1785 - H1792. [Abstract] [Full Text] [PDF]
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E. Takimoto, D. G. Soergel, P. M.L. Janssen, L. B. Stull, D. A. Kass, and A. M. Murphy Frequency- and Afterload-Dependent Cardiac Modulation In Vivo by Troponin I With Constitutively Active Protein Kinase A Phosphorylation Sites Circ. Res., March 5, 2004; 94(4): 496 - 504. [Abstract] [Full Text] [PDF]
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E. E. J. M. Creemers, J. N. Davis, A. M. Parkhurst, P. Leenders, K. B. Dowdy, E. Hapke, A. M. Hauet, P. G. Escobar, J. P. M. Cleutjens, J. F. M. Smits, et al. Deficiency of TIMP-1 exacerbates LV remodeling after myocardial infarction in mice Am J Physiol Heart Circ Physiol, January 1, 2003; 284(1): H364 - H371. [Abstract] [Full Text] [PDF]
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S. Nemoto, G. DeFreitas, D. L. Mann, and B. A. Carabello Effects of changes in left ventricular contractility on indexes of contractility in mice Am J Physiol Heart Circ Physiol, December 1, 2002; 283(6): H2504 - H2510. [Abstract] [Full Text] [PDF]
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J. N. Lorenz A practical guide to evaluating cardiovascular, renal, and pulmonary function in mice Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2002; 282(6): R1565 - R1582. [Abstract] [Full Text] [PDF]
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P. Steendijk, E. Staal, J. W. Jukema, and J. Baan Hypertonic saline method accurately determines parallel conductance for dual-field conductance catheter Am J Physiol Heart Circ Physiol, August 1, 2001; 281(2): H755 - H763. [Abstract] [Full Text] [PDF]
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P. A. White, C. I. O. Brookes, H. Ravn, V. Hjortdal, R. R. Chaturvedi, and A. N. Redington Validation and utility of novel volume reduction technique for determination of parallel conductance Am J Physiol Heart Circ Physiol, January 1, 2001; 280(1): H475 - H482. [Abstract] [Full Text] [PDF]
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, derivation data set; 
, validation.
Covariance analysis revealed no significant difference in the
regressions for the 2 data sets. The combined regression was highly
significant, with a slope and intercept minimally different from the
line of identity. B: analysis of difference
[Vp(DF) 
