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Intracellular calcium and myocardial function during ischemia
D G Allen1, S P Cairns, S E Turvey
1Department of Physiology, University of Sydney, NSW, Australia.
Insights
Cardiac ischemia impairs heart muscle function due to reduced protein responsiveness, not calcium release. Increased intracellular calcium during reperfusion correlates with muscle damage.
Area of Science:
- Cardiology
- Biochemistry
- Physiology
Background:
- Cardiac ischemia leads to rapid mechanical dysfunction and cell death upon reperfusion.
- Early mechanical decline may stem from altered intracellular calcium or myofibrillar protein sensitivity.
- Intracellular calcium levels rise during ischemia, impacting cardiac function.
Purpose of the Study:
- To elucidate the mechanisms behind the early decline in cardiac mechanical performance during ischemia.
- To investigate the roles of intracellular calcium, protons, and phosphate in myocardial dysfunction.
Main Methods:
- Analysis of intracellular ion concentrations (calcium, sodium) and pH during ischemic events.
- Assessment of myofibrillar protein responsiveness to calcium under varying conditions.
- Correlation of reperfusion calcium levels with myocardial damage.
Main Results:
- The early decline in mechanical performance is primarily attributed to inhibitory effects of phosphate and protons on myofibrillar proteins.
- Intracellular calcium increases during ischemia, driven by sodium influx via the Na/Ca exchanger, itself triggered by Na/H exchanger activity.
- Elevated intracellular calcium during reperfusion is closely correlated with the extent of myocardial damage.
Conclusions:
- Myocardial dysfunction during early ischemia is mainly due to impaired myofibrillar protein function caused by acidosis and phosphate accumulation.
- Intracellular calcium overload during reperfusion exacerbates myocardial injury.
Abstract:
Cardiac ischemia causes a rapid decline in mechanical performance and, if prolonged, myocardial cell death occurs on reperfusion. The early decline in mechanical performance could, in principle, be caused either by reduced intracellular calcium release or by reduced responsiveness of the myofibrillar proteins to calcium. It is now known that intracellular calcium rises during ischemia and that the early decline in mechanical performance is caused largely by the inhibitory effects of phosphate and protons on the myofibrillar proteins. The rise of intracellular calcium during ischemia is related to the acidosis and is probably caused by calcium influx on the Na/Ca exchanger. This is triggered by a rise in intracellular sodium which enter the cell in exchange for protons on the Na/H exchanger. Intracellular calcium rises still further on reperfusion the elevation of calcium and the degree of muscle damage are closely correlated.