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Cardiac injury in short duration anoxia and modification by diltiazem, a calcium channel blocking agent
Abstract:
The protective effects of diltiazem were studied in isolated perfused rat hearts after 10, 20 and 30 minutes of anoxia and 10 minutes of reoxygenation. The hearts were treated with diltiazem, 4 mg/liter, during anoxia and reoxygenation. The myocardial tissue was processed for electron microscopy and tissue calcium was measured. Four types of cell injury ranging from normal to severe were observed. The prominent morphologic changes in the nondiltiazem-treated tissue were contraction bands, distortion and calcification of mitochondria and loss of glycogen. In the treated group, a partial reduction of cell injury was noted. The mitochondria were usually well preserved, but contraction bands were present. The tissue calcium decreased after treatment with diltiazem. The observations suggest that diltiazem decreases tissue calcium and protects mitochondria more than other cellular components against calcium overload, and this protection may be responsible for the beneficial action of this drug.
Insights
Diltiazem treatment reduced cell injury in rat hearts during anoxia and reoxygenation. This calcium channel blocker protected mitochondria and decreased tissue calcium levels, suggesting a beneficial effect.
Area of Science:
- Cardiovascular Pharmacology
- Cellular Biology
- Ischemic Heart Disease Research
Background:
- Anoxia and reoxygenation induce significant myocardial cell injury.
- Calcium overload is a key factor in ischemic heart damage.
- Diltiazem is a calcium channel blocker with potential cardioprotective properties.
Purpose of the Study:
- To investigate the protective effects of diltiazem on isolated perfused rat hearts subjected to anoxia and reoxygenation.
- To evaluate the impact of diltiazem on myocardial cell morphology and tissue calcium levels.
- To elucidate the mechanism underlying diltiazem's potential cardioprotection.
Main Methods:
- Isolated perfused rat hearts were exposed to anoxia (10, 20, 30 minutes) followed by reoxygenation (10 minutes).
- Hearts were treated with diltiazem (4 mg/liter) during anoxia and reoxygenation.
- Myocardial tissue was analyzed using electron microscopy and tissue calcium measurements.
Main Results:
- Untreated hearts showed severe cell injury, including contraction bands, mitochondrial distortion/calcification, and glycogen loss.
- Diltiazem-treated hearts exhibited partially reduced cell injury with better mitochondrial preservation.
- Tissue calcium levels were decreased in the diltiazem-treated group.
Conclusions:
- Diltiazem demonstrates cardioprotective effects against anoxia-reoxygenation injury in rat hearts.
- The drug reduces tissue calcium overload and protects mitochondria.
- Preservation of mitochondria and reduced calcium overload likely contribute to diltiazem's beneficial actions in cardiac ischemia.