Myocardial VO2 of mechanically unloaded contraction of rat ventricular slices measured by a new approach

1996 ◽  
Vol 270 (3) ◽  
pp. H1063-H1070 ◽  
Author(s):  
S. Yasuhara ◽  
M. Takaki ◽  
A. Kikuta ◽  
H. Ito ◽  
H. Suga
Keyword(s):  
Electrical Field Stimulation ◽  
Left Ventricular ◽  
Tyrode Solution ◽  
Electrical Field ◽  
New Approach ◽  
Contraction Coupling ◽  
Cross Bridge ◽  
Butanedione Monoxime ◽  
Normal Inhibition ◽  
Normal Tyrode Solution

We instituted a new approach of measuring mechanically unloaded myocardial oxygen consumption (VO2) by using rat left ventricular (LV) slices in an air-tight chamber filled with oxygenated Tyrode solution. Myocardial slices (300 microns in thickness) freely shortened without external load by electrical field stimulation (St). VO2 without St (n = 6) was 1.69 +/- 0.41 ml O2.min-1.100 g LV-1. VO2 with St (n = 6) increased to 2.28 +/- 0.36 ml O2.min-1.100 g LV-1. VO2 in Ca(2+)-free Tyrode solution irrespective of St was nearly equal to VO2 without St in normal Tyrode solution, indicating that all these VO2 correspond to basal metabolic VO2. The increment in VO2 by St (delta VO2) increased up to twice normal with the extracellular Ca2+ concentration up to 4 times normal. Inhibition of cross-bridge cycling by 2,3-butanedione monoxime (5 and 10 mM) did not decrease delta VO2. These results suggest that delta VO2 consists of VO2 primarily for excitation-contraction coupling but not for cross-bridge cycling.

O2 consumption of mechanically unloaded contractions of mouse left ventricular myocardial slices

2004 ◽  
Vol 287 (1) ◽  
pp. H54-H62 ◽  
Author(s):  
Daisuke Yamashita ◽  
Hisaharu Kohzuki ◽  
Yutaka Kitagawa ◽  
Tamiji Nakashima ◽  
Akio Kikuta ◽  
...  
Keyword(s):  
Cyclopiazonic Acid ◽  
Left Ventricular ◽  
Dependent Manner ◽  
O2 Consumption ◽  
Tyrode Solution ◽  
Independent Manner ◽  
Contraction Coupling ◽  
Butanedione Monoxime ◽  
Dose Dependent ◽  
Normal Tyrode Solution

Left ventricular (LV) myocardial slices were isolated from murine hearts (300 μm thick) and were stimulated at 1 Hz without external load. Mean myocardial slice O2 consumption (MVo2) per minute (mMVo2) without stimulation was 0.97 ± 0.14 ml O2·min−1·100 g LV−1 and mean mMVo2 with stimulation increased to 1.80 ± 0.17 ml O2·min−1·100 g LV−1 in normal Tyrode solution. Mean ΔmVo2 (the mMVo2 with stimulation − the mMVo2 without stimulation) was 0.83 ± 0.12 ml O2·min−1·100 g LV−1. There were no differences between mean mMVo2 with and without stimulation in Ca2+-free solution. The increases in extracellular Ca2+ concentrations up to 14.4 mM did not affect the mMVo2 without stimulation but significantly increased the mMVo2 with stimulation up to 140% of control. The ΔmMVo2 significantly increased up to 190% of the control in a dose-dependent manner. In contrast, the shortening did not increase in a dose-dependent manner. Cyclopiazonic acid (CPA; 30 μM) significantly reduced the ΔmMVo2 to 0.27 ± 0.06 ml O2·min−1·100 g LV−1 (35% of control). The combination of 5 mM 2,3-butanedione monoxime (BDM) and 30 μM CPA did not further decrease ΔmMVo2. Although BDM (3–5 mM) decreased the ΔmMVo2 by 28–30% of control in a dose-independent manner, 3–5 mM BDM decreased shortening in a dose-dependent manner. Our results indicate that the ΔmMVo2 of mouse LV slices during shortening under mechanically unloaded conditions consists of energy expenditure for total Ca2+ handling during excitation-contraction coupling, basal metabolism, but no residual cross-bridge cycling.

scholarly journals Energy expenditure by Ba2+contracture in rat ventricular slices derives from cross-bridge cycling

1999 ◽  
Vol 277 (1) ◽  
pp. H74-H79 ◽  
Author(s):  
Hisaharu Kohzuki ◽  
Hiromi Misawa ◽  
Susumu Sakata ◽  
Yoshimi Ohga ◽  
Hiroyuki Suga ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Energy Expenditure ◽  
Cyclopiazonic Acid ◽  
Left Ventricular ◽  
Basal Metabolism ◽  
Dependent Manner ◽  
Tyrode Solution ◽  
Cross Bridge ◽  
Butanedione Monoxime ◽  
Dose Dependent

To clarify the energy-expenditure mechanism during Ba2+ contracture of mechanically unloaded rat left ventricular (LV) slices, we measured myocardial O2 consumption (V˙o 2) of quiescent slices in Ca2+-free Tyrode solution andV˙o 2 during Ba2+ contracture by substituting Ca2+ with Ba2+. We then investigated the effects of cyclopiazonic acid (CPA) and 2,3-butanedione monoxime (BDM) on the Ba2+ contractureV˙o 2. The Ca2+-freeV˙o 2 corresponds to that of basal metabolism (2.32 ± 0.53 ml O2 ⋅ min−1 ⋅ 100 g LV−1). Ba2+ increased theV˙o 2 in a dose-dependent manner (from 0.3 to 3.0 mmol/l) from 110 to 150% of basal metabolic V˙o 2. Blockade of the sarcoplasmic reticulum (SR) Ca2+ pump by CPA (10 μmol/l) did not at all decrease the Ba2+-activatedV˙o 2. BDM (5 mmol/l), which specifically inhibits cross-bridge cycling, reduced the Ba2+activatedV˙o 2 almost to basal metabolic V˙o 2. These energetic results revealed that the Ba2+-activatedV˙o 2 was used for the cross-bridge cycling but not for the Ca2+ handling by the SR Ca2+ pump.

scholarly journals Positive Inotropic Effects of ATP Released via the Maxi-Anion Channel in Langendorff-Perfused Mouse Hearts Subjected to Ischemia-Reperfusion

2021 ◽  
Vol 9 ◽  
Author(s):  
Hiroshi Matsuura ◽  
Akiko Kojima ◽  
Yutaka Fukushima ◽  
Yu Xie ◽  
Xinya Mi ◽  
...  
Keyword(s):  
Contractile Function ◽  
Organic Anion ◽  
Left Ventricular ◽  
Transient Increase ◽  
Tyrode Solution ◽  
Inotropic Effects ◽  
Cl Channel ◽  
Short Period ◽  
Cl Channels ◽  
Normal Tyrode Solution

The organic anion transporter SLCO2A1 constitutes an essential core component of the ATP-conductive large-conductance anion (Maxi-Cl) channel. Our previous experiments using Langendorff-perfused mouse hearts showed that the Maxi-Cl channel contributes largely to the release of ATP into the coronary effluent observed during 10-min reperfusion following a short period (6 min) of oxygen-glucose deprivation. The present study examined the effect of endogenous ATP released via Maxi-Cl channels on the left ventricular contractile function of Langendorff-perfused mouse hearts, using a fluid-filled balloon connected to a pressure transducer. After the initial 30-min stabilization period, the heart was then perfused with oxygen-glucose-deprived Tyrode solution for 6 min, which was followed by a 10-min perfusion with oxygenated normal Tyrode solution in the absence and presence of an ATP-hydrolyzing enzyme, apyrase, and/or an adenosine A1 receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). In the absence of apyrase and DPCPX, the left ventricular developed pressure (LVDP) decreased from a baseline value of 72.3 ± 7.1 to 57.5 ± 5.5 mmHg (n = 4) at the end of 6-min perfusion with oxygen-glucose-deprived Tyrode solution, which was followed by a transient increase to 108.5 ± 16.5 mmHg during subsequent perfusion with oxygenated normal Tyrode solution. However, in the presence of apyrase and DPCPX, the LVDP decreased to the same degree during 6-min perfusion with oxygen-glucose-deprived Tyrode solution, but failed to exhibit a transient increase during a subsequent perfusion with oxygenated normal Tyrode solution. These results strongly suggest that endogenous ATP released through Maxi-Cl channels contributes to the development of transient positive inotropy observed during reperfusion after short-period hypoxia/ischemia in the heart.

Cross-bridge dephosphorylation and relaxation of vascular smooth muscle

1989 ◽  
Vol 256 (2) ◽  
pp. C282-C287 ◽  
Author(s):  
C. M. Hai ◽  
R. A. Murphy
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Time Course ◽  
Electrical Field Stimulation ◽  
Shortening Velocity ◽  
Electrical Field ◽  
Cross Bridge ◽  
Time Course Data ◽  
Necessary And Sufficient ◽  
Isotonic Shortening

We tested the hypothesis that relaxation in vascular smooth muscle is the result of inactivation of myosin light chain kinase and cross-bridge dephosphorylation. Fast neurally mediated contractions of swine carotid medial strips were induced by electrical field stimulation. Termination of the stimulus resulted in relaxation with a half time of 2 min. Nifedipine (0.1 microM) increased the relaxation rate without significant effects on the contractile response. Cross-bridge dephosphorylation was much faster than stress decay with basal levels reached within 1 min when 73% of the developed stress remained. The time-course data of dephosphorylation and stress were analyzed with a model that predicted the dependences of stress and isotonic shortening velocity on cross-bridge phosphorylation during contraction. Rate constants resolved from contraction data also fitted the relaxation data when the model's prediction was corrected for estimated errors in the phosphorylation measurements. Because Ca2+-dependent cross-bridge phosphorylation was the only postulated regulatory mechanism in the model, these results are consistent with the hypothesis that cross-bridge dephosphorylation is necessary and sufficient to explain relaxation in the swine carotid media.

Electrically stimulated contraction accelerates protein synthesis rates in adult feline cardiocytes

1993 ◽  
Vol 265 (2) ◽  
pp. H666-H674 ◽  
Author(s):  
C. T. Ivester ◽  
R. L. Kent ◽  
H. Tagawa ◽  
H. Tsutsui ◽  
T. Imamura ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Electrical Stimulation ◽  
Total Protein ◽  
Actinomycin D ◽  
Electrical Field Stimulation ◽  
Cell Protein ◽  
Electrical Field ◽  
Butanedione Monoxime ◽  
H Protein ◽  
Stimulation Of

Cardiocytes were induced to contract via electrical field stimulation with an 8 V/cm electrical square-wave pulse of 5 ms at 0.125-2.0 Hz for up to 6 h. Protein synthesis rates were measured as rate of incorporation of [3H]-phenylalanine into total cell protein. Rates of protein synthesis were accelerated 43 +/- 4%, P < 0.001, by 4 h. The acceleration of total protein synthesis showed a frequency dependence between 0.125 and 0.5 Hz. In addition to accelerating rates of total protein synthesis, electrical stimulation of contraction accelerated fractional rates of synthesis of myosin heavy chain by 42 +/- 8%, P < 0.05. Protein synthesis rates were not accelerated upon electrical stimulation using subthreshold voltages. Addition of 100 ng/ml of actinomycin D had no effect on the ability of electrical stimulation of contraction to accelerate protein synthesis. To uncouple excitation-contraction coupling, 2,3-butanedione monoxime (BDM) was used to block actin-myosin cross-bridge interactions. BDM significantly decreased the ability of electrical stimulation to accelerate protein synthesis rates.

Ca(2+)-free, high-Ca2+ coronary perfusion suppresses contractility and excitation-contraction coupling energy

1995 ◽  
Vol 268 (3) ◽  
pp. H1061-H1070 ◽  
Author(s):  
J. Araki ◽  
M. Takaki ◽  
T. Namba ◽  
M. Mori ◽  
H. Suga
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Ultrastructural Changes ◽  
Coronary Perfusion ◽  
Oxygen Cost ◽  
Tyrode Solution ◽  
Coupling Energy ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Contractile Failure

We studied the mechanoenergetic effects of a short-term Ca(2+)-free, high-Ca2+ Tyrode solution coronary perfusion in eight excised, cross-circulated canine hearts. The perfusion protocol consisted of coronary perfusion with Ca(2+)-free Tyrode solution for 10 min followed by high-Ca2+ (16 mM) Tyrode solution for 5 min. This new protocol successfully induced acute contractile failure in seven hearts, without myocardial ultrastructural changes. We studied the end-systolic pressure-volume relation (slope = Emax, a contractility index) and the relation between oxygen consumption per beat (VO2) and systolic pressure-volume area (PVA) in these failing hearts. These hearts had no increase in end-diastolic pressure at a given volume, a 40% decrease in Emax and a proportional decrease in the PVA-independent VO2 for 1–4 h, but no decrease in the oxygen cost of PVA, defined as the slope of the VO2-PVA relation. The oxygen cost of Emax for Ca2+ handling, defined as the slope of the relation between PVA-independent VO2 and Emax, was unchanged in the failing hearts. We conclude that the present protocol induced left ventricular contractile failure, primarily involving the suppression of Ca2+ handling energy for excitation-contraction coupling.

Pre- and postjunctional effects of a thromboxane mimetic in canine bronchi

1991 ◽  
Vol 261 (4) ◽  
pp. L271-L276 ◽  
Author(s):  
L. J. Janssen ◽  
E. E. Daniel
Keyword(s):  
Mechanical Response ◽  
Thromboxane A2 ◽  
Electrical Field Stimulation ◽  
Tetraacetic Acid ◽  
Electrical Field ◽  
Contraction Coupling ◽  
Intracellular Ca ◽  
Excitatory Junction Potentials ◽  
Thromboxane Receptors ◽  
Free Media

Thromboxane A2 is believed to participate in causation of hyperreactivity of airway smooth muscle (ASM). We therefore investigated the effects of a thromboxane mimetic (U-46619) on isolated ring segments of canine bronchial ASM (3rd to 5th order). U-46619 (10(-9)-10(-5) M) was found to elicit tonic contraction, membrane depolarization, and oscillations in membrane potential. These effects were sensitive to blockade of thromboxane receptors (using 10(-8) M L 670, 596); the mechanical response was insensitive to 3 x 10(-8) M atropine, 10(-7) M nitrendipine, or exposure to Ca(2+)-free media [(containing 0.5 mM ethylene glycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA)]. U-46619 also potentiated electrical field stimulation-elicited contractions and excitatory junction potentials without altering the sensitivity to carbachol. This potentiation was also sensitive to L 670,596 but not to blockade of adrenoceptors (using phentolamine plus propranolol). We conclude that canine bronchial ASM possesses both prejunctional and postjunctional thromboxane receptors. The former potentiate cholinergic neurotransmission through a mechanism not involving adrenoceptors. The latter excite the ASM through a mechanism not involving muscarinic receptors and that utilizes intracellular Ca2+ (rather than extracellular Ca2+). Excitation-contraction coupling was found to be pharmacomechanical in nature (rather than electromechanical).

An ultrastructural analysis of the sympathetic innervation of the rabbit ear artery and middle cerebral artery and their branches

1992 ◽  
Vol 50 (1) ◽  
pp. 934-935
Author(s):  
John T. Dodge ◽  
John A. Bevan
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Sympathetic Innervation ◽  
Electrical Field Stimulation ◽  
Rabbit Ear Artery ◽  
Electrical Field ◽  
Functional Differences ◽  
Ear Artery ◽  
Rabbit Ear ◽  
Vascular Beds

Unlike many peripheral vascular beds, the sympathetic nervous system exerts little control on cerebral blood flow. The contractile response of isolated rabbit middle cerebral artery (MCA) segments to electrical field stimulation of its intramural nerves is less than in a similar-sized artery from the ear. This study was undertaken to characterize and compare the perivascular neuromuscular relationships and innervation density of similar-sized arteries varying in diameter from these two different regional arterial beds to see if there were structural correlates for these functional differences.

An approach for comparative quantification of myocardial blood flow (0-15-H2O-PET), perfusion (Tc-99m-tetrofosmin-SPECT), and metabolism (F 18-FDG-PET)

2001 ◽  
Vol 40 (05) ◽  
pp. 164-171 ◽  
Author(s):  
B. Nowak ◽  
H.-J. Kaiser ◽  
S. Block ◽  
K.-C. Koch ◽  
J. vom Dahl ◽  
...  
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Fdg Pet ◽  
Model Fitting ◽  
Compartment Model ◽  
Left Ventricular ◽  
Short Axis ◽  
New Approach ◽  
Single Compartment Model ◽  
Tissue Fraction

Summary Aim: In the present study a new approach has been developed for comparative quantification of absolute myocardial blood flow (MBF), myocardial perfusion, and myocardial metabolism in short-axis slices. Methods: 42 patients with severe CAD, referred for myocardial viability diagnostics, were studied consecutively with 0-15-H2O PET (H2O-PET) (twice), Tc-99m-Tetrofosmin 5PECT (TT-SPECT) and F-18-FDG PET (FDG-PET). All dato sets were reconstructed using attenuation correction and reoriented into short axis slices. Each heart was divided into three representative slices (base, rnidventricular, apex) and 18 ROIs were defined on the FDG PET images and transferred to the corresponding H2O-PET and TT-SPECT slices. TT-SPECT and FDG-PET data were normalized to the ROI showing maximum perfusion. MBF was calculated for all left-ventricular ROIs using a single-compartment-model fitting the dynamic H2O-PET studies. Microsphere equivalent MBF (MBF_micr) was calculated by multiplying MBF and tissue-fraction, a parameter which was obtained by fitting the dynamic H2O-PET studies. To reduce influence of viability only well perfused areas (>70% TT-SPECT) were used for comparative quantification. Results: First and second mean global MBF values were 0.85 ml × min-1 × g-1 and 0.84 ml × min-1 × g1, respectively, with a repeatability coefficient of 0.30 ml ÷ min-1 × gl. After sectorization mean MBF_micr was between 0.58 ml × min1 ÷ ml"1 and 0.68 ml × min-1 × ml"1 in well perfused areas. Corresponding TT-SPECT values ranged from 83 % to 91 %, and FDG-PET values from 91 % to 103%. All procedures yielded higher values for the lateral than the septal regions. Conclusion: Comparative quantification of MBF, MBF_micr, TT-SPECT perfusion and FDG-PET metabolism can be done with the introduced method in short axis slices. The obtained values agree well with experimentally validated values of MBF and MBF_micr.

scholarly journals Remodeling of t-system and proteins underlying excitation-contraction coupling in aging versus failing human heart

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yankun Lyu ◽  
Vipin K. Verma ◽  
Younjee Lee ◽  
Iosif Taleb ◽  
Rachit Badolia ◽  
...  
Keyword(s):  
Heart Function ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Excitation Contraction Coupling ◽  
Transverse Tubular System ◽  
Contraction Coupling ◽  
Senescent Phenotype ◽  
Cellular Microstructure ◽  
T System

AbstractIt is well established that the aging heart progressively remodels towards a senescent phenotype, but alterations of cellular microstructure and their differences to chronic heart failure (HF) associated remodeling remain ill-defined. Here, we show that the transverse tubular system (t-system) and proteins underlying excitation-contraction coupling in cardiomyocytes are characteristically remodeled with age. We shed light on mechanisms of this remodeling and identified similarities and differences to chronic HF. Using left ventricular myocardium from donors and HF patients with ages between 19 and 75 years, we established a library of 3D reconstructions of the t-system as well as ryanodine receptor (RyR) and junctophilin 2 (JPH2) clusters. Aging was characterized by t-system alterations and sarcolemmal dissociation of RyR clusters. This remodeling was less pronounced than in HF and accompanied by major alterations of JPH2 arrangement. Our study indicates that targeting sarcolemmal association of JPH2 might ameliorate age-associated deficiencies of heart function.

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