GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    Abstract 540: Magnesium Improves Cardiac Diastolic Function by Modulating Mitochondria
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Circulation Research Vol. 123, No. Suppl_1 ( 2018-08-03)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 123, No. Suppl_1 ( 2018-08-03)
    Abstract: Rationale: A diet rich in saturated fat has been found to induce diabetes mellitus (DM) accompanied by myocardial mitochondrial dysfunction, insulin resistance, and magnesium (Mg) deficiency. The most prominent characteristic of diabetic cardiomyopathy is cardiac diastolic dysfunction (DD). Mg supplementation improves the heart rate variability and arterial elasticity in chronic heart failure. Recently, we have reported that mitochondrial reactive oxygen species (mitoROS) play a critical role in the progress of DD and diastolic heart failure. Therefore, we hypothesized that Mg supplementation would benefit diastolic function by improving mitochondrial function. Methods and Results: High fat diet (HFD)-induced diabetic mouse hearts showed cardiac DD with increased E/e’ (45±2 in DM mice vs. 32±2 in control mice), increased left ventricular diastolic volume (LVDV, 80±1 μL in DM vs. 61±4 μL in control), and increased incidence of DD (9 of 10 mice in DM vs 1 of 10 mice in control; P 〈 0.05 for all). DM mice also showed decreased plasma Mg concentration (0.80±0.04 mmol/L in DM vs. 0.98±0.03 mmol/L in control, P 〈 0.05). Ventricular cardiomyocytes isolated from DM mice exhibited decreased mitochondrial ATP production (75±11% of control), a 1.7±0.2-fold increase in mitoROS, significantly depolarized mitochondrial membrane potential, and mitochondrial Ca 2+ overload (3.7±1.3-fold; P 〈 0.05 vs. control for all). Dietary Mg administration (50 mg/mL, ≈6-8 g/kg/day) for 6 weeks corrected all these parameters with increased plasma Mg concentration (1.5±0.1 mmol/L), improved cardiac diastolic function (E/e’ 37±1; LVDV 54±5 μL; LVPWT 0.77±0.02 mm; the incidence of DD, 2 of 10 mice; P 〈 0.05 vs. DM for all). Mitochondrial function was improved significantly by Mg with increased ATP production, decreased mitoROS, repolarized mitochondrial membrane potential, and decreased mitochondrial Ca 2+ overload in DM mice. Conclusion: These results indicate that Mg supplementation improved mitochondrial function, reduced oxidative stress, and prevented diastolic dysfunction in DM.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.123.suppl_1.540
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 1467838-X
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Ranolazine Improves Cardiac Diastolic Dysfunction Through Modulation of Myofilament Calcium Sensitivity
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Circulation Research Vol. 110, No. 6 ( 2012-03-16), p. 841-850
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 110, No. 6 ( 2012-03-16), p. 841-850
    Abstract: Previously, we demonstrated that a deoxycorticosterone acetate (DOCA)-salt hypertensive mouse model produces cardiac oxidative stress and diastolic dysfunction with preserved systolic function. Oxidative stress has been shown to increase late inward sodium current (I Na ), reducing the net cytosolic Ca 2+ efflux. Objective: Oxidative stress in the DOCA-salt model may increase late I Na , resulting in diastolic dysfunction amenable to treatment with ranolazine. Methods and Results: Echocardiography detected evidence of diastolic dysfunction in hypertensive mice that improved after treatment with ranolazine (E/E′:sham, 31.9±2.8, sham+ranolazine, 30.2±1.9, DOCA-salt, 41.8±2.6, and DOCA-salt+ranolazine, 31.9±2.6; P =0.018). The end-diastolic pressure-volume relationship slope was elevated in DOCA-salt mice, improving to sham levels with treatment (sham, 0.16±0.01 versus sham+ranolazine, 0.18±0.01 versus DOCA-salt, 0.23±0.2 versus DOCA-salt+ranolazine, 0.17±0.0 1 mm Hg/L; P 〈 0.005). DOCA-salt myocytes demonstrated impaired relaxation, τ, improving with ranolazine (DOCA-salt, 0.18±0.02, DOCA-salt+ranolazine, 0.13±0.01, sham, 0.11±0.01, sham+ranolazine, 0.09±0.02 seconds; P =0.0004). Neither late I Na nor the Ca 2+ transients were different from sham myocytes. Detergent extracted fiber bundles from DOCA-salt hearts demonstrated increased myofilament response to Ca 2+ with glutathionylation of myosin binding protein C. Treatment with ranolazine ameliorated the Ca 2+ response and cross-bridge kinetics. Conclusions: Diastolic dysfunction could be reversed by ranolazine, probably resulting from a direct effect on myofilaments, indicating that cardiac oxidative stress may mediate diastolic dysfunction through altering the contractile apparatus.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.111.258251
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 1467838-X
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    PLASMA CARDIAC MYOSIN BINDING PROTEIN-C MAY BE A NOVEL BIOMARKER FOR HEART FAILURE
    Elsevier BV ; 2015
    In:  Journal of the American College of Cardiology Vol. 65, No. 10 ( 2015-03), p. A993-
    Details
    In: Journal of the American College of Cardiology, Elsevier BV, Vol. 65, No. 10 ( 2015-03), p. A993-
    Type of Medium: Online Resource
    ISSN: 0735-1097
    URL: Article
    DOI: 10.1016/S0735-1097(15)60993-7
    RVK:
    XA 17760
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2015
    detail.hit.zdb_id: 1468327-1
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    Abstract P240: Mitochondrial Reactive Oxygen Species Regulate the Cardiac Na + Channel in Heart Failure
    Ovid Technologies (Wolters Kluwer Health) ; 2011
    In:  Circulation Research Vol. 109, No. suppl_1 ( 2011-12-09)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 109, No. suppl_1 ( 2011-12-09)
    Abstract: Background: Previously, we have shown that elevated intracellular NADH causes a decrease in cardiac Na + current ( I Na ) signaled by an increase in mitochondrial reactive oxygen species (ROS). The decrease in I Na can be ameliorated by NAD + or a mitochondrial specific anti-oxidant, mitoTEMPO. It is known that cardiomyopathy is associated with reduced I Na . Therefore, we tested whether the NADH-mitochondrial ROS pathway was involved in the reduction in I Na in cardiomyopathic mice. Methods: Nonischemic cardiomyopathy was induced in C57BL/6 mice 6 weeks after unilateral nephrectomy, deoxycorticosterone acetate (DOCA) pellet implantation, and salt water substitution. Sham operated mice were used as controls. Ventricular myocytes isolated from mice were utilized for whole-cell patch clamp recording, intracellular NADH/NAD + level measurements, and mitochondrial ROS monitoring with confocal microscopy. Results: Compared to the sham mice, the left ventricular volume was significantly enlarged (105.5 ± 4.4 µL vs. 91.6 ± 4.0 µL, P 〈 0.05), and the ejection fraction was significantly reduced (39.2 ± 1.6% vs. 48.7 ± 1.6%, P 〈 0.05) in DOCA mice. Intracellular NADH level was increased (2.78-fold; P 〈 0.01), and I Na was decreased (62±8%; P 〈 0.01) in myocytes of DOCA mice vs. sham. NAD + (500 μ M) and mitoTEMPO (10 μ M) recovered I Na (90±9% and 103±9% of sham, respectively, P 〉 0.05). Mitochondrial ROS overproduction was observed with DOCA mice myocytes by MitoSOX Red (∼4.8-fold of sham; P 〈 0.01). NAD + and mitoTEMPO decreased ROS in DOCA mice myocytes (∼20±6% of DOCA for both, P 〈 0.01). Conclusions: NADH and mitochondrial ROS were elevated, and I Na was decreased in nonischemic cardiomyopathy. Maneuvers that reduced mitochondrial ROS restored I Na . Since reduced I Na and the subsequent slow conduction velocity are thought to contribute to arrhythmic risk in this condition, NAD + and mitochondrial anti-oxidants may have anti-arrhythmic activity in cardiomyopathy.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.109.suppl_1.AP240
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2011
    detail.hit.zdb_id: 1467838-X
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...