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Effects of calcium chloride administration on the postischemic isolated rat heart
1Department of Surgery, West Virginia University Medical Center, Morgantown.
Insights
Early calcium administration during heart reperfusion worsens ventricular dysfunction and mitochondrial damage. Delaying calcium allows for improved heart function, highlighting the importance of normocalcemic reperfusion.
Area of Science:
- Cardiovascular Physiology
- Mitochondrial Biology
- Ischemic Heart Disease
Background:
- Hypercalcemic reperfusion post-ischemia is linked to ventricular dysfunction.
- Mitochondrial ultrastructural changes are observed in the postischemic heart.
Purpose of the Study:
- To correlate ventricular function, mitochondrial damage, and high-energy phosphate levels with calcium levels during reperfusion.
- To determine the optimal timing for calcium administration during postischemic reperfusion.
Main Methods:
- Utilized an isolated working rat heart model.
- Administered calcium chloride at varying times and concentrations during reperfusion.
- Assessed ventricular function, mitochondrial integrity, and adenosine triphosphate (ATP) levels.
Main Results:
- Early calcium administration caused dose-dependent ventricular dysfunction and increased mitochondrial damage.
- Delayed calcium administration (after 15 minutes of normocalcemic reperfusion) augmented cardiac function.
- Hearts receiving early calcium showed reduced ATP stores compared to delayed administration groups.
Conclusions:
- A period of normocalcemic reperfusion is critical before calcium administration in the postischemic heart.
- Mitochondrial damage and subsequent decreased ATP synthesis likely underlie the ventricular dysfunction observed with early hypercalcemic reperfusion.
Abstract:
Hypercalcemic reperfusion of the postischemic heart has been associated with ventricular dysfunction and with ultrastructural changes in the mitochondria. The isolated working rat heart model was used to correlate ventricular function, mitochondrial damage, and high-energy phosphate content with degree and timing of hypercalcemia during reperfusion. When administered early during reperfusion, calcium chloride caused a dose-dependent deterioration in ventricular function, whereas calcium augmented function when it was administered after a 15-minute period of normocalcemic reperfusion. Hearts treated with calcium early during reperfusion demonstrated more mitochondrial damage and decreased stores of adenosine triphosphate than those in which calcium administration was delayed. The data indicate that a period of normocalcemic reperfusion should precede calcium administration in the postischemic heart. Mitochondrial damage resulting in decreased synthesis of adenosine triphosphate is likely the cause of ventricular dysfunction associated with calcium administration in the postischemic heart.