Cardiac contractile dysfunction during mild coronary flow reductions is due to an altered calcium-pressure relationship in rat hearts.

Figueredo, Vincent M.; Brandes, Rolf; Weiner, Michael W.; Massie, Barry M.; Camacho, S. Albert

doi:10.1172/jci116054

Cited by 31 publications

(9 citation statements)

References 31 publications

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“…The isovolumic heart preparation has been described in detail previously (19,20). Isolated hearts were perfused using a KrebsHenseleit (KH) buffer containing (mmol/liter): NaCl (118), KCl (6.0), MgSO 4 (1.2), CaCl 2 (2.0), NaHCO 3 (25), pyruvate (5.0), glucose (4.0), insulin 20 U/liter and 95% O 2 -5% CO 2 (37 Њ C, pH of 7.35-7.45). Hearts were paced at 5 Hz.…”

Section: Methodsmentioning

confidence: 99%

“…Potential sources of artifact were accounted for and/or minimized (heart motion [23], autofluorescence [21,22] unhydrolyzed indo-1 AM [24], tissue filter effect [21,22], and potential loading of indo-1 into endothelial cells or noncytosolic compartments [25,26] Myocyte isolation and preparation of myocyte homogenates. After hemodynamic and fluorescence measurements, myocytes were isolated with collagenase (27).…”

Section: Methodsmentioning

confidence: 99%

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Thyroid hormone improves function and Ca2+ handling in pressure overload hypertrophy. Association with increased sarcoplasmic reticulum Ca2+-ATPase and alpha-myosin heavy chain in rat hearts.

Chang¹,

Figueredo²,

Schreur³

et al. 1997

J. Clin. Invest.

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We asked whether thyroid hormone (T 4 ) would improve heart function in left ventricular hypertrophy (LVH) induced by pressure overload (aortic banding). After banding for 10-22 wk, rats were treated with T 4 or saline for 10-14 d. Isovolumic LV pressure and cytosolic [Ca 2 ϩ ] (indo-1) were assessed in perfused hearts. Sarcoplasmic reticulum Ca 2 ϩ -ATPase (SERCA), phospholamban, and ␣ -and ␤ -myosin heavy chain (MHC) proteins were assayed in homogenates of myocytes isolated from the same hearts. Of 14 banded hearts treated with saline, 8 had compensated LVH with normal function (LVH comp ), whereas 6 had abnormal contraction, relaxation, and calcium handling (LVH decomp ). In contrast, banded animals treated with T 4 had no myocardial dysfunction; these hearts had increased contractility, and faster relaxation and cytosolic [Ca

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Thyroid hormone improves function and Ca2+ handling in pressure overload hypertrophy. Association with increased sarcoplasmic reticulum Ca2+-ATPase and alpha-myosin heavy chain in rat hearts.

Chang¹,

Figueredo²,

Schreur³

et al. 1997

J. Clin. Invest.

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“…Of those few studies addressing adenosine-mediated inotropy, some use low to moderate levels of perfusion (e.g. 60 mmHg pressure in the murine study of Tikh et al [47]; <10 ml min −1 g −1 flow in the rat study of Marin and Franchini [34]) that have been previously shown to limit inotropic and/or energy state in mouse [20], rat [7,14] and guinea pig hearts [1]. It is therefore difficult to interpret inotropic effects of AR agonism under these conditions.…”

Section: Ar-mediated Functional Changes and The Gregg Phenomenon A Kementioning

confidence: 99%

Contractile effects of adenosine, coronary flow and perfusion pressure in murine myocardium

Willems

Headrick

2006

Pflugers Arch - Eur J Physiol

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There is mixed evidence adenosine receptors (ARs) may enhance myocardial contractility, although this remains contentious. We assessed inotropic actions of adenosine (50 muM) and selective AR activation with 100 nM N (6)-cyclohexyladenosine (CHA; A(1)AR agonist), 25 nM 2-[p-(2-carboxyethyl) phenethylamino]-5'-N-ethylcarboxamidoadenosine (CGS-21680; A(2A)AR agonist) and 100 nM 2-chloro-N (6)-(3-iodobenzyl)-adenosine-5'-N-methyluronamide (Cl-IB-MECA; A(3)AR agonist) in mouse hearts perfused at constant pressure, constant flow, or conditions of stable flow and pressure (following maximal nitroprusside-mediated dilatation at constant flow). Adenosine and CGS-21680 significantly (although modestly) increased force in constant-pressure perfused hearts (

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“…The central role of free cytosolic [Ca2+] ([Ca2+]C) in excitation-contraction coupling of cardiac myocytes has led to the development of several techniques to measure [Ca2+]c in a variety of experimental preparations. In isolated whole hearts, [Ca2+]c has been measured using the fluorescent indicators indo-1 (Lee et al, 1988;Wikman-Coffelt et al, 1991;Figueredo et al, 1992) and fura-2 (Ataka et al, 1992), the bioluminescent protein aequorin (Kihara et al, 1989), and 19F-BAPTA NMR (Steenbergen et al, 1987;Kitakaze and Marban, 1989). Each of these techniques has advantages and limitations.…”

Section: Introductionmentioning

confidence: 99%

Cytosolic and mitochondrial [Ca2+] in whole hearts using indo-1 acetoxymethyl ester: effects of high extracellular Ca2+

Schreur

Figueredo

Miyamae

et al. 1996

Biophysical Journal

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Assessment of free cytosolic [Ca2+] ([Ca2+]c) using the acetoxymethyl ester (AM) form of indo-1 may be compromised by loading of indo-1 into noncytosolic compartments, primarily mitochondria. To determine the fraction of noncytosolic fluorescence in whole hearts loaded with indo-1 AM, Mn2+ was used to quench cytosolic fluorescence. Residual (i.e., noncytosolic) fluorescence was subtracted from the total fluorescence before calculating [Ca2+]c. Noncytosolic fluorescence was used to estimate mitochondrial [Ca2+]. In hearts paced at 5 Hz (N = 17), noncytosolic fluorescence was 0.61 +/- 0.06 and 0.56 +/- 0.07 of total fluorescence at lambda 385 and lambda 456, respectively. After taking into account noncytosolic fluorescence, systolic and diastolic [Ca2+]c was 673 +/- 72 and 132 +/- 9 nM, respectively, noncytosolic [Ca2+] was 183 +/- 36 nM and increased to 272 +/- 12 when extracellular Ca2+ was increased from 2 to 6 mM. This increase in noncytosolic [Ca2+] was inhibited by ruthenium red, a blocker of Ca2+ uptake by mitochondria. We conclude that cytosolic and mitochondrial [Ca2+] can be determined in whole hearts loaded with indo-1 AM by using Mn2+ to quench cytosolic fluorescence.

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Cardiac contractile dysfunction during mild coronary flow reductions is due to an altered calcium-pressure relationship in rat hearts.

Cited by 31 publications

References 31 publications

Thyroid hormone improves function and Ca2+ handling in pressure overload hypertrophy. Association with increased sarcoplasmic reticulum Ca2+-ATPase and alpha-myosin heavy chain in rat hearts.

Thyroid hormone improves function and Ca2+ handling in pressure overload hypertrophy. Association with increased sarcoplasmic reticulum Ca2+-ATPase and alpha-myosin heavy chain in rat hearts.

Contractile effects of adenosine, coronary flow and perfusion pressure in murine myocardium

Cytosolic and mitochondrial [Ca2+] in whole hearts using indo-1 acetoxymethyl ester: effects of high extracellular Ca2+

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