Effect of calcium chloride administration on the postischemic isolated rat heart
Albert Abbott1, Ronald Hill1, Larry Shears1
1Department of Surgery, West Virginia University Medical Center, Morgantown, West Virginia USA.
Insights
Early calcium administration during heart reperfusion worsens ventricular dysfunction and mitochondrial damage. Delaying calcium improves heart function, suggesting normocalcemic reperfusion is crucial for postischemic recovery.
Area of Science:
- Cardiovascular Physiology
- Mitochondrial Biology
- Ischemic Heart Disease
Background:
- Hypercalcemic reperfusion can impair postischemic heart function.
- Mitochondrial ultrastructural changes are observed following ischemia and reperfusion.
- High-energy phosphate levels are critical for cardiac contractility.
Purpose of the Study:
- To investigate the relationship between calcium administration timing during reperfusion and cardiac function.
- To correlate ventricular dysfunction with mitochondrial damage and high-energy phosphate content.
- To determine the optimal timing for calcium administration in the postischemic heart.
Main Methods:
- Utilized an isolated working rat heart model.
- Manipulated the timing and dosage of calcium chloride during reperfusion.
- Assessed ventricular function, mitochondrial integrity, and adenosine triphosphate (ATP) levels.
Main Results:
- Early calcium administration caused dose-dependent ventricular dysfunction.
- Delayed calcium administration (after 15 minutes of normocalcemic reperfusion) augmented cardiac function.
- Hearts receiving early calcium showed increased mitochondrial damage and reduced ATP stores.
Conclusions:
- A period of normocalcemic reperfusion is recommended before calcium administration in postischemic hearts.
- Mitochondrial damage and subsequent decreased ATP synthesis likely underlie calcium-induced ventricular dysfunction.
- Timing of calcium administration is a critical factor in managing postischemic cardiac recovery.
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.
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