Electrophysiologic and mechanical properties of single feline RV and LV myocytes

Kleiman, Robert B.; Houser, Steven R.

doi:10.1016/0022-2828(88)90575-5

Cited by 9 publications

(11 citation statements)

References 22 publications

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“…This is similar to previous reports in different species including the guinea pig, 16,17 rabbits 6 and cats. 18 In rodents, a larger density of the Ca 2+ -independent transient outward K + current I to has been reported in RV, with a corresponding shorter APD. 19,20 In canine hearts, epicardial LV and RV APDs are similar; however a larger I to in RV leads to a more prominent phase 1 notch in action potentials recorded in RV myocytes.…”

Section: Discussionmentioning

confidence: 92%

Left-to-right ventricular differences in IKATP underlie epicardial repolarization gradient during global ischemia

et al. 2011

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Background The ionic mechanisms of electrical heterogeneity in the ischemic ventricular epicardium remain poorly understood. Objective To test the hypothesis that the ATP-activated K+ current (IKATP) plays an important role in mediating repolarization differences between the right (RV) and left ventricle (LV) during global ischemia. Methods Electrical activity in Langendorff-perfused guinea pig hearts was recorded optically during control, ischemia, and reperfusion. Patch-clamp experiments were used to quantify IKATP density in isolated myocytes. Molecular correlates of IKATP (Kir6/SUR) were probed via RT-PCR. The role of IKATP in modulating repolarization was studied using computer simulations. Results Action potential duration (APD) was similar between LV and RV in controls, but significantly different in global ischemia. Pre-treatment of hearts with 10 μM glibenclamide (IKATP blocker) abolished the APD gradient during ischemia. In the absence of ischemia, pinacidil (IKATP opener) tended to shorten the APD more in the LV, and caused a small but significant increase in APD dispersion. In voltage clamp experiments, the density of the whole-cell current activated by pinacidil at depolarized potentials was significantly larger in LV, compared with RV epicardial myocytes. The mRNA levels of Kir6.1/Kir6.2 were significantly higher in LV, compared to RV. Simulations showed that IKATP is the main determinant of LV-RV APD gradient, whereas cell-to-cell coupling modified the spatial distribution of this APD gradient. Conclusion IKATP is an important determinant of the epicardial LV-RV APD gradient during global ischemia, in part due to a higher current density and molecular expression in the LV.

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Section: Discussionmentioning

confidence: 92%

Left-to-right ventricular differences in IKATP underlie epicardial repolarization gradient during global ischemia

et al. 2011

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“…There appear to be species differences in this behaviour, however, as a converse result was obtained in mouse myocytes (Kondo et al . 2006), and a null result was found in cat myocytes (Kleiman & Houser, 1988). Since the seminal publication by Bárány (1967), it has been known that shortening velocity is correlated with the Ca 2+ ‐triggered, actin‐activated ATPase activity of myosin.…”

Section: Discussionmentioning

confidence: 99%

“…Both trabeculae (Gruver et al . 1994) and myocytes (Kleiman & Houser, 1988) isolated from either ventricle have the same twitch characteristics. RV and LV tissues (Smolich et al .…”

Section: Introductionmentioning

confidence: 98%

Interventricular comparison of the energetics of contraction of trabeculae carneae isolated from the rat heart

Han

Taberner

Nielsen

et al. 2013

The Journal of Physiology

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Key points• With each beat of the heart, the left and right ventricles must overcome substantially different arterial pressures in order to eject blood.• We have tested whether this difference in mechanical demand is reflected in different metabolic energy expenditure.• Our experimental preparations were trabeculae isolated from both ventricles; our index of metabolic energy expenditure was their heat production in response to electrical stimulation.• We found that the cost of activating contraction (i.e. the production of heat in the absence of force generation) was higher in trabeculae from the left ventricle, thereby conferring a lower mechanical efficiency on that ventricle.• Correction for the activation heat reveals the thermodynamic efficiency of the actomyosin crossbridges; whereas there was no interventricular difference in this fundamental property of cardiac muscle, its dependence on force development is baffling.Abstract We compare the energetics of right ventricular and left ventricular trabeculae carneae isolated from rat hearts. Using our work-loop calorimeter, we subjected trabeculae to stress-length work (W ), designed to mimic the pressure-volume work of the heart. Simultaneous measurement of heat production (Q) allowed calculation of the accompanying change of enthalpy ( H = W + Q). From the mechanical measurements (i.e. stress and change of length), we calculated work, shortening velocity and power. In combination with heat measurements, we calculated activation heat (Q A ), crossbridge heat (Q xb ) and two measures of cardiac efficiency: 'mechanical efficiency' (ε mech = W / H) and 'crossbridge efficiency' (ε xb = W /( H -Q A )). With respect to their left ventricular counterparts, right venticular trabeculae have higher peak shortening velocity, and higher peak mechanical efficiency, but with no difference of stress development, twitch duration, work performance, shortening power or crossbridge efficiency. That is, the 35% greater maximum mechanical efficiency of right venticular than left ventricular trabeculae (13.6 vs. 10.2%) is offset by the greater metabolic cost of activation (Q A ) in the latter. When corrected for this difference, crossbridge efficiency does not differ between the ventricles.

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“…42 Cardiomyocyte shortening and relaxation rate in RV and LV were also similar in cats. 43 Interestingly, interventricular differences in RyR2 expression were eliminated, and total RyR2 expression decreased in dogs with arrhythmogenic right ventricular cardiomyopathy. 41 Similarly, Gupta et al 44 found reduced SERCA2a activity and protein levels in LV, but not RV, in dogs with chronic heart failure, eliminating interventricular differences.…”

Section: Differences In Ca 2+ Handling and Contractilitymentioning

confidence: 99%

Differences in Left Versus Right Ventricular Electrophysiological Properties in Cardiac Dysfunction and Arrhythmogenesis

Molina

Heijman

Dobrev

2016

Arrhythmia &Amp; Electrophysiology Review

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Optimal cardiac function depends on appropriate rate and force of contraction, with specific cardiac regions having developed particular beat-to-beat properties depending on their individual functions. For example, isovolumetric contraction time is shorter in the right ventricle (RV) than in the left ventricle (LV). At the cellular level, cardiac function is regulated by regional cardiomyocyte electrophysiological and Ca 2+ -handling properties (see Figure 1). Differences in these properties between nodal cells and working myocardium, 1,2 atrial and ventricular cardiomyocytes 1,3,4 and different layers of the LV wall (endo-, mid-and epicardium) [5][6][7] have been well established. Although electrophysiological differences between left and right sides of the heart have been less extensively characterised there is evidence for clinically relevant left-toright differences in the atrium 1,[8][9][10] and the ventricle. 1,5,[11][12][13][14] Here, we review the known differences in LV and RV electrophysiology and Ca 2+ handling at baseline and during pathophysiological conditions. Furthermore, we discuss the implications of these differences for arrhythmogenesis. Basic Cardiac Electrophysiology and Arrhythmia MechanismsCardiac excitation-contraction (EC) coupling is a sequence of events occurring in cardiomyocytes upon electrical activation, resulting in the generation of an action potential (AP) and subsequent cardiomyocyte contraction (see Figure 2). This sequence shows many similarities between different cell types, notably between LV and RV cardiomyocytes.In this section we briefly summarise the common features. Figure 2A). Moreover, the Ca 2+ entering the cardiomyocyte through L-type Ca 2+ channels plays a critical role initiating EC coupling by activating type-2 ryanodine receptor (RyR2) channels on the sarcoplasmic reticulum (SR) membrane, producing a much larger SR Ca 2+ release. This process is termed Ca 2+ -induced Ca 2+ release (CICR) and results in an increase in the cytoplasmic Ca 2+ concentration sufficient to activate the contractile apparatus, initiating cardiomyocyte contraction. 15 Subsequently, resequestration of Ca 2+ in the SR by the SR Ca 2+ ATPase type-2a (SERCA2a) and extrusion of Ca 2+ to the extracellular space by the Na + -Ca 2+ exchanger type-1 (NCX1) returns cytosolic Ca 2+ to diastolic levels, promoting cellular relaxation. Finally, ionic homeostasis of intracellular Na + and K + is maintained by the Na + / Abstract A wide range of ion channels, transporters, signaling pathways and tissue structure at a microscopic and macroscopic scale regulate the electrophysiological activity of the heart. Each region of the heart has optimised these properties based on its specific role during the cardiac cycle, leading to well-established differences in electrophysiology, Ca 2+ handling and tissue structure between atria and ventricles and between different layers of the ventricular wall. Similarly, the right ventricle (RV) and left ventricle (LV) have different embryological, structural, metabol...

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Electrophysiologic and mechanical properties of single feline RV and LV myocytes

Cited by 9 publications

References 22 publications

Left-to-right ventricular differences in IKATP underlie epicardial repolarization gradient during global ischemia

Left-to-right ventricular differences in IKATP underlie epicardial repolarization gradient during global ischemia

Interventricular comparison of the energetics of contraction of trabeculae carneae isolated from the rat heart

Differences in Left Versus Right Ventricular Electrophysiological Properties in Cardiac Dysfunction and Arrhythmogenesis

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