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Excitation-contraction coupling in hypothermic ischemic myocardium
The American Journal of Physiology
|March 1, 1981
Summary
Global ischemia in hypothermic hearts impairs sarcoplasmic reticulum calcium uptake and myofibrillar function. Despite preserved glycogen stores, these defects in excitation-contraction coupling may explain reduced heart function after reperfusion.
Area of Science:
- Cardiology
- Biochemistry
- Physiology
Background:
- Global ischemia and hypothermia significantly impact myocardial function.
- Understanding the excitation-contraction coupling system is crucial for cardiac health.
Purpose of the Study:
- To investigate the functional integrity of the sarcoplasmic reticulum (SR) and myofibrils in hypothermic ischemic myocardium.
- To determine the impact of global ischemia on glycogen stores and calcium handling within the heart.
Main Methods:
- Surgically induced global ischemia in hypothermic myocardium.
- Evaluation of isolated sarcoplasmic reticulum (SR) and myofibril function.
- Measurement of calcium uptake, SR Ca2+-ATPase activity, and myofibrillar pCa-ATPase activity.
- Determination of myocardial glycogen decay over 30 and 60 minutes.
Main Results:
- SR calcium uptake was significantly depressed in ischemic groups compared to controls.
- SR Ca2+-ATPase activity remained unchanged, indicating preserved enzyme function.
- Myofibrillar pCa-ATPase activity was depressed, with increased Km, suggesting impaired contractility.
- Glycogen decay was depressed, indicating preserved glycogen stores.
Conclusions:
- Hypothermic ischemic myocardium exhibits impaired SR calcium transport and reduced myofibrillar ATPase activity.
- Preserved SR Ca2+-ATPase and adequate glycogen stores contrast with functional deficits.
- These excitation-contraction coupling defects likely contribute to depressed myocardial function post-reperfusion.