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Wall tension and myocardial dysfunction after ischemia and reperfusion
1Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06510.
The American Journal of Physiology
|February 1, 1993
Summary
Mechanical stress during heart ischemia significantly worsens damage. Even mild pressure on an ischemic heart segment reduces functional recovery and depletes energy stores, unlike in non-contracting isolated hearts.
Area of Science:
- Cardiology
- Physiology
- Biochemistry
Background:
- Cell viability is preserved in isolated ischemic hearts due to lack of mechanical function (acute hibernation).
- Noncontracting ischemic heart segments in vivo sustain irreversible damage within 30 minutes.
Purpose of the Study:
- To investigate the impact of mechanical stress on ischemic myocardium.
- To compare the effects of varying ventricular pressures on heart function and metabolism during ischemia.
Main Methods:
- Isolated rabbit hearts underwent 90 minutes of ischemia with controlled coronary flow.
- Ventricular balloon pressure was elevated to simulate dyskinetic segment stress.
- Systolic function, tissue ATP, glycogen, and oxygen consumption were assessed post-reperfusion.
Main Results:
- Elevated ventricular pressure during ischemia significantly reduced recovery of peak systolic pressure.
- Higher pressures and longer durations of stress led to greater functional and metabolic deterioration.
- Tissue ATP and glycogen levels were significantly reduced, and myocardial oxygen consumption decreased.
Conclusions:
- Mechanical stress, mimicking dyskinetic segments, exacerbates metabolic and functional decline in ischemic myocardium.
- The absence of mechanical stress is crucial for preserving cell viability during prolonged ischemia in isolated heart models.