What question did this study set out to answer?

To determine whether myofibrillar damage and impaired ATPase activity contribute to contractile dysfunction in rat hearts undergoing calcium-paradox injury.

February 17, 2017Molecular and Cellular BiochemistryOpen Access

Myosin heavy chain and cardiac troponin T damage is associated with impaired myofibrillar ATPase activity contributing to sarcomeric dysfunction in Ca2+-paradox rat hearts

Q: What is the clinical evidence from this study?

Study design: Other. Population: Ca2+-paradox (Ischemia/Reperfusion Injury Model) (n=24). Intervention: Ca2+-paradox (Ca2+-depletion followed by repletion) vs. Normal Krebs-Henseleit medium (Control). Primary outcome: Left ventricular developed pressure (LVDP) (p=<0.001).

View Full Paper

Ask AI

Bookmark

Key result

Ca2+-paradox significantly reduced left ventricular developed pressure to 12.9 mmHg compared to 127.4 mmHg in control rat hearts, associated with decreased Ca2+-stimulated ATPase activity.

Population

Isolated male Sprague-Dawley rat hearts (250-300 g) and isolated cardiomyocytes

Comparison

Ca2+-depletion for 5 min followed by… vs Control hearts perfused with normal…

Design

Preclinical, randomized into three groups

Follow-up

15 minutes

Authors

ÁKÁrṕad Kov́acsRuhr University Bochum JKJudit KalászUniversity of Debrecen EPEnikő T. PásztorUniversity of Debrecen

Discussion

Member takes

Implication

Implicates sarcomeric ATPase impairment in rat contractile failure; hypothesis-generating for human calcium paradox mechanisms.

Key Points

To determine whether myofibrillar damage and impaired ATPase activity contribute to contractile dysfunction in rat hearts undergoing calcium-paradox injury.
Perfused isolated rat hearts using the Langendorff apparatus under three successive conditions: baseline Krebs–Henseleit buffer (Control), Ca2+-depletion, and Ca2+-repletion (Ca2+-paradox).
Recorded hemodynamic performance (LVDP, LVEDP, and ±dP/dt), evaluated single-cardiomyocyte mechanics (active tension and rate of force redevelopment ktr,max), and quantified myofibrillar Ca2+- and Mg2+-ATPase activities alongside α-myosin heavy chain and cardiac troponin T degradation.
Left ventricular developed pressure dropped from 127.4 ± 6.1 mmHg in controls to 9.8 ± 1.3 mmHg during Ca2+-depletion and 12.9 ± 1.3 mmHg during Ca2+-paradox, accompanied by increased end-diastolic pressure and steep reductions in ±dP/dt.
Ca2+-stimulated myofibrillar ATPase activity declined in Ca2+-paradox hearts compared to controls (8.40 ± 0.22 vs. 12.08 ± 0.57 µmol Pi/mg protein/h), while Mg2+-ATPase activity increased (7.21 ± 0.36 vs. 3.20 ± 0.25 µmol Pi/mg protein/h).
Isolated cardiomyocytes from Ca2+-paradox hearts exhibited diminished active tension (12.12 ± 3.19 vs. 25.07 ± 3.51 kN/m2) and reduced ktr,max (3.21 ± 23 vs. 4.61 ± 22), matching progressive degradation of α-myosin heavy chain and cardiac troponin T.

Structured PICO

Population

Isolated male Sprague-Dawley rat hearts (250-300 g) and isolated cardiomyocytes

Intervention

Ca2+-depletion for 5 min followed by Ca2+-repletion for 10 min (Ca2+-paradox) via Langendorff perfusion

Comparator

Control hearts perfused with normal Krebs-Henseleit solution containing 1.25 mM Ca2+ for 15 min

Outcome

Left ventricular developed pressure (LVDP), end-diastolic pressure (LVEDP), +dP/dt, -dP/dt, myofibrillar ATPase activity, and cardiomyocyte force generationsurrogate

Main Result

Absolute Event Rate: 12.9% vs 127.4%

p-value: p=<0.001

Contractile impairment in Ca2+-paradox rat hearts is partially driven by deranged sarcomeric function and compromised myofibrillar ATPase activity due to degradation of α-myosin heavy chain and cardiac troponin T.

Cite This Study

Kov́acs et al. (2017) studied Ca2+-paradox (Ischemia/Reperfusion Injury Model) (n=24). Ca2+-paradox (Ca2+-depletion followed by repletion) vs. Normal Krebs-Henseleit medium (Control) was evaluated on Left ventricular developed pressure (LVDP) (p=<0.001). Ca2+-paradox significantly reduced left ventricular developed pressure to 12.9 mmHg compared to 127.4 mmHg in control rat hearts, associated with decreased Ca2+-stimulated ATPase activity.

synapsesocial.com/papers/6a1c6eec973ffece4bc3cf7a https://doi.org/10.1007/s11010-017-2954-8

View Full Paper

Ask AI

Bookmark

Myosin heavy chain and cardiac troponin T damage is associated with impaired myofibrillar ATPase activity contributing to sarcomeric dysfunction in Ca2+-paradox rat hearts

Discussion

Member takes

Implication

Key Points

Structured PICO

Main Result

Cite This Study

Myosin heavy chain and cardiac troponin T damage is associated with impaired myofibrillar ATPase activity contributing to sarcomeric dysfunction in Ca2+-paradox rat hearts

Discussion

Member takes

Implication

Key Points

Structured PICO

Main Result

Cite This Study

Also Consider

Also Consider