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Changes in contractile function and endogenous fuel supply in rat heart upon perfusion with substrate-free medium
Advances in Myocardiology
|January 1, 1980
Summary
Heart contractile failure during substrate-free perfusion is linked to impaired glycogen and triglyceride mobilization, and reduced ATP generation and utilization. This leads to metabolic dysfunction and loss of function.
Area of Science:
- Cardiovascular Physiology
- Metabolic Biochemistry
Background:
- Cardiac function relies on continuous energy supply.
- Understanding metabolic shifts during energy substrate deprivation is crucial for cardiac health.
Purpose of the Study:
- To investigate the functional and metabolic changes in isolated rat hearts perfused with substrate-free medium.
- To identify the key metabolic factors contributing to contractile failure.
Main Methods:
- Isolated rat hearts were perfused with aerobic substrate-free medium.
- Functional parameters (contractile force, resting tension) and metabolic intermediates (glycogen, ATP, CrP, etc.) were measured over 120 minutes.
Main Results:
- Contractile force declined after 30 minutes, preceding significant drops in glycogen, phosphate potential, and creatine phosphate.
- Early failure (30-60 min) showed increased free fatty acid (FFA) and AMP; late failure (90-120 min) showed increased resting tension and decreased oxygen consumption.
- Complete failure occurred with substantial glycogen, ATP, creatine phosphate, and triglyceride reserves remaining.
Conclusions:
- Contractile failure in this model is not solely due to substrate depletion but also impaired endogenous energy mobilization and ATP metabolism.
- Insufficiency in mobilizing glycogen and triglycerides, alongside issues in ATP generation/utilization, likely drives failure.