What does this research mean for the field?

Ischemia-induced myocardial contracture and impaired diastolic relaxation are closely driven by the accumulation of intracellular calcium, a process that can be prevented by the calcium antagonist nifedipine. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To investigate the relationship between intracellular calcium accumulation in mitochondria and the development of myocardial contracture and diastolic dysfunction during ischemia and reperfusion.

December 1, 1977AJP Heart and Circulatory Physiology

Myocardial contracture and accumulation of mitochondrial calcium in ischemic rabbit heart

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Why the study?

Does nifedipine prevent myocardial contracture and mitochondrial calcium accumulation in isolated ischemic rabbit hearts?

Population

Electrically paced, isolated perfused rabbit hearts

Comparison

Nifedipine (10(-7) M) vs Ischemia without nifedipine

Design

Preclinical

Follow-up

60 min ischemia with or without 10 min reperfusion

Authors

PHPeter J. HenryJames Madison University RSR. Schuchleib JDJ. W. DavisDuke Medical Center

Discussion

Member takes

Implication

Protects against ischemic contracture and mitochondrial calcium overload in rabbit hearts; leaves open clinical translation to reperfusion injury.

Key Points

To investigate the relationship between intracellular calcium accumulation in mitochondria and the development of myocardial contracture and diastolic dysfunction during ischemia and reperfusion.
Electrically paced, isolated perfused rabbit hearts were subjected to 60 minutes of low-flow ischemia with or without 10 minutes of high-flow reperfusion.
Contractility and stiffness were assessed via isovolumic left ventricular dP/dt and end-diastolic pressure, with intracellular calcium measured in the mitochondrial fraction in the presence or absence of nifedipine (10⁻⁷ M).
Low-flow ischemia caused ventricular standstill and contracture, while reperfusion yielded only partial mechanical recovery and persistently elevated end-diastolic pressure.
Increases in mitochondrial calcium closely paralleled the severity of contracture and the failure of diastolic relaxation following reperfusion.
Nifedipine (10⁻⁷ M) prevented ischemic contracture, halted mitochondrial calcium accumulation, and enabled near-complete mechanical recovery without elevated diastolic pressure.

Structured PICO

Does nifedipine prevent myocardial contracture and mitochondrial calcium accumulation in isolated ischemic rabbit hearts?

Population

Electrically paced, isolated perfused rabbit hearts

Intervention

Nifedipine (10(-7) M)

Comparator

Ischemia without nifedipine

Outcome

Myocardial contracture (isovolumic left ventricular dP/dt and end-diastolic pressure) and mitochondrial calcium accumulationsurrogate

Nifedipine prevents myocardial contracture and mitochondrial calcium accumulation during ischemia and reperfusion in isolated rabbit hearts.

Cite This Study

Henry et al. (1977) studied this question.

synapsesocial.com/papers/6a1a2f039b2d28adb7b4fa3a https://doi.org/10.1152/ajpheart.1977.233.6.h677

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Implication

Protects against ischemic contracture and mitochondrial calcium overload in rabbit hearts; leaves open clinical translation to reperfusion injury.

Myocardial contracture and accumulation of mitochondrial calcium in ischemic rabbit heart

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Myocardial contracture and accumulation of mitochondrial calcium in ischemic rabbit heart

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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