Direct recording of EDP-EDV relationship in isolated rat left ventricle: effect of diastolic crossbridge formation

Schiereck, P.; Hoefnagel, R; Beer, E. L. de; Heijst, Bas G. V. Van; Mosterd, W. L.

doi:10.1093/cvr/28.5.715

Cited by 9 publications

(4 citation statements)

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“…Our acquisition of the parallel conductance (Vp) was according to a method reported in large animals rst by Baan [7] and more recently in rats by Schiereck [17]. The conductivity of the blood was momentarily altered without affecting the LV volume or contractile properties of the left ventricle.…”

Section: Parallel Conductancementioning

confidence: 99%

Validation of Conductance Catheter System for Quantification of Murine Pressure-Volume Loops

Yang

Larson

Beischel

et al. 2001

Journal of Investigative Surgery

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The purpose of this study was to define the validation methods and outcomes of a conductance catheter system specifically for in vivo murine cardiac hemodynamic analysis. To express the relationship between conductance and blood volumes, we used an in vitro model to derive a volume-conductance line. The volume-conductance line was used to compute raw volume from the modified conductance signals. The parallel volume was calibrated with hypertonic (15%) saline injected from extrajugular vein. The ventricular volume was computed by raw volume minus parallel volume. The accuracy of conductance volumetric measurements was validated with a static in situ infusion of calibrated volumes of whole blood injected into arrested left ventricles. In vivo dynamic measurements were performed with 24 C57B1/6 mice, 6 months old; for comparison of established values. The in situ model showed that after calibration, the experimental coefficient, alpha, was equal to 1 and the measured volume by conductance catheter was equal to the true volume of the left ventricle (y = 0.982x + 0.513, p < .0001). For the in vivo models, the end-diastolic volumes and the stroke volumes and cardiac output determined with the conductance catheter system were 17.3 +/- 1.0 microL, 10.6 +/- 0.9 microL, and 6.0 +/- 0.5 mL/min, respectively. We validated the relationship between measured volume by conductance catheter and the true volume and demonstrated the accuracy of the volume-conductance line for conversion of conductance to volume.

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Section: Parallel Conductancementioning

confidence: 99%

Validation of Conductance Catheter System for Quantification of Murine Pressure-Volume Loops

Yang

Larson

Beischel

et al. 2001

Journal of Investigative Surgery

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“…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).…”

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confidence: 99%

Estimation of parallel conductance by dual-frequency conductance catheter in mice

Georgakopoulos

Kass

2000

American Journal of Physiology-Heart and Circulatory Physiology

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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 (V(p)) 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 V(p) derived by hypertonic saline injection was consistent [0.095 +/- 0.01 (SD), n = 11], and both methods were strongly correlated (r(2) = 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 V(p(DF)) = 1.1 * V(p(Sal)) - 2.5 [where V(p(DF)) is V(p) derived by the dual-frequency method and V(p(Sal)) is V(p) derived by hypertonic saline bolus injection], r(2) = 0.95, standard error of the estimate = 1.1 microl, and mean difference = 0.6 +/- 1.4 microl. Varying V(p(Sal)) in a given animal resulted in parallel changes in V(p(DF)) (multiple regression r(2) = 0.92, P < 0.00001). The dominant source of V(p) 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 V(p) and flow probe-derived cardiac output, end-diastolic volume and ejection fraction in normal mice were 28 +/- 3 microl 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.

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“…In systole, the cross-bridge cycling rate and force generation increase in relation to the magnitude of the cytosolic calcium transient and the sensitivity of myofibrillar regulatory proteins to calcium (8). In diastole, there is an active reuptake of calcium into the sarcoplasmic reticulum; however, a low level of calcium-activated crossbridge cycling and active tension development may persist at end diastole (17). Thus, whereas end-diastolic ventricular pressure-dimension relations are generally considered to reflect the underlying passive material properties of cardiac muscle (13), it is possible that changes in calcium availability or myofilament calcium sensitivity influence these relations.…”

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confidence: 99%

“…It is also supported by studies (12,19) in isolated resting cardiac myocytes demonstrating that cell length increases when intracellular calcium concentration is reduced or when myofilament calcium sensitivity is reduced by 2,3-butanedione monoxime (BDM). Furthermore, studies in isolated nonworking hearts demonstrate that treatment with a calcium channel antagonist (17) or BDM (20) produces a rightward shift in the left ventricular (LV) end-diastolic pressure (EDP)-volume relation. By analogy, if both systolic and end-diastolic calcium availability or myofilament calcium sensitivity are reduced in vivo, then coordinate changes in systolic function and end-diastolic muscle length would be predicted.…”

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confidence: 99%

A common mechanism for concurrent changes of diastolic muscle length and systolic function in intact hearts

Zhu

et al. 2001

American Journal of Physiology-Heart and Circulatory Physiology

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Mechanical properties of the myocardium at end diastole have been thought to be dominated by passive material properties rather than by active sarcomere cross-bridge interactions. This study tested the hypothesis that residual cross-bridges significantly contribute to end-diastolic mechanics in vivo and that changes in end-diastolic cross-bridge interaction parallel concurrent changes in systolic cross-bridge interaction. Open-chest anesthetized pigs were treated with intracoronary verapamil (n = 7) or 2,3-butanedione monoxime (BDM; n = 8). Regional left ventricular external work and end-diastolic pressure (EDP) versus end-diastolic segment length (EDL) relations were determined in the treated and untreated regions of each heart. Both agents reduced external work of treated regions to 31-38% of baseline and concurrently shifted EDP versus EDL relations to the right (i.e., greater EDL at a given EDP) by an average of 5% (P < 0.05). During washout of the drugs, EDP versus EDL returned to baseline in parallel with recovery of external work. Sarcomere length, measured by transmission electron microscopy in BDM-treated and untreated regions of the same hearts after diastolic arrest and perfusion fixation, was 8% greater in BDM-treated regions (P < 0.01). We concluded that residual diastolic cross-bridges significantly and reversibly influence end-diastolic mechanics in vivo. Alterations of end-diastolic and systolic cross-bridge interactions occur in parallel. Keywordsdiastole; ventricular function; calcium channel blockers; di-acetyl analogs and derivatives; sarcomeres Cross-bridge cycling triggered by the presence of cytosolic calcium is the basis for force generation in muscle. In systole, the cross-bridge cycling rate and force generation increase in relation to the magnitude of the cytosolic calcium transient and the sensitivity of myofibrillar regulatory proteins to calcium (8). In diastole, there is an active reuptake of calcium into the sarcoplasmic reticulum; however, a low level of calcium-activated crossbridge cycling and active tension development may persist at end diastole (17). Thus, whereas end-diastolic ventricular pressure-dimension relations are generally considered to reflect the underlying passive material properties of cardiac muscle (13), it is possible that changes in calcium availability or myofilament calcium sensitivity influence these relations. This concept is supported by a study (5) in isolated spontaneously beating cardiac myocytes demonstrating that cell length continues to increase throughout diastole. It is also supported by studies (12,19) Recent data from our laboratory support such a prediction. In a porcine model of acute myocardial ischemia and reperfusion resulting in systolic dysfunction (stunning), we observed increased end-diastolic segment length (EDL) at low EDP in vivo and increased diastolic sarcomere length after in situ perfusion fixation at low LV cavity pressure (15). These increases in end-diastolic muscle length and diastolic sarcomere length occurred in ...

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Direct recording of EDP-EDV relationship in isolated rat left ventricle: effect of diastolic crossbridge formation

Abstract: At low EDP, diastolic volume is dependent upon weakly bound crossbridges as a function of the [Ca2+] in the cardiac cell.

Cited by 9 publications

References 0 publications

Validation of Conductance Catheter System for Quantification of Murine Pressure-Volume Loops

Validation of Conductance Catheter System for Quantification of Murine Pressure-Volume Loops

Estimation of parallel conductance by dual-frequency conductance catheter in mice

A common mechanism for concurrent changes of diastolic muscle length and systolic function in intact hearts

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