What question did this study set out to answer?

To evaluate the alterations in oxidative phosphorylation and respiratory control across various exogenous carbon substrates following myocardial ischemia and reperfusion.

July 1, 1989Journal of Biological ChemistryOpen Access

Alterations in Oxidative Function and Respiratory Regulation in the Post-ischemic Myocardium

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To evaluate the alterations in oxidative phosphorylation and respiratory control across various exogenous carbon substrates following myocardial ischemia and reperfusion.
Perfused normal and post-ischemic isovolumic rat hearts using a Langendorff preparation with either glucose and insulin, palmitate and glucose, or pyruvate and glucose.
Subjected hearts to normothermic ischemia at 38 °C until the onset of ischemic contracture followed by reperfusion.
Monitored phosphorus-31 nuclear magnetic resonance (31P NMR) spectra, free ADP levels, and mechanical function across varying myocardial oxygen consumption rates (MVO2).
Free ADP levels were significantly decreased after ischemia, and respiratory regulation shifted from an ADP-independent state to an ADP:Pi-limited domain in hearts perfused with glucose plus insulin or palmitate plus glucose.
In the pyruvate plus glucose group, respiration operated in the ADP:Pi-limited domain both before and after ischemia, but the apparent Km relating MVO2 to ADP was significantly decreased post-reperfusion.
Maximal oxidative capacity (Vmax for MVO2) was substantially diminished across all substrate conditions, directly constraining maximal post-ischemic mechanical performance.

Structured PICO

Population

Isovolumic Langendorff perfused rat hearts

Intervention

Ischemia at 38 degrees C until the onset of ischemic contracture and subsequent reperfusion, perfused with different exogenous carbon sources (glucose and insulin, palmitate and glucose, or pyruvate and glucose)

Comparator

Normal (control) perfused rat hearts

Outcome

31P NMR spectra, mechanical performance, and "free" ADP levels relative to myocardial oxygen consumption rates (MVO2)surrogate

Ischemia and reperfusion in rat hearts significantly reduce post-ischemic oxidative capacity and alter the kinetic regulation of oxidative phosphorylation, which limits maximal post-ischemic mechanical performance.

Discussion

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Implication

May constrain post-ischemic recovery in rodent models; leaves open translation to human reperfusion injury mechanisms.

Cite This Study

Zimmer et al. (1989) studied this question.

synapsesocial.com/papers/6a7c1d31af1d6cbe7375d5da https://doi.org/10.1016/s0021-9258(18)63873-6

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Alterations in Oxidative Function and Respiratory Regulation in the Post-ischemic Myocardium

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Alterations in Oxidative Function and Respiratory Regulation in the Post-ischemic Myocardium

Key Points

Structured PICO

Discussion

Implication

Cite This Study

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