Author + information
- Received July 15, 1982
- Revision received October 28, 1982
- Accepted November 5, 1982
- Published online April 1, 1983.
- Pacha Meyian Rahamathulla, BVSc, PhD,
- Muhammad Ashraf, PhD*,
- Arnold Schwartz, PhD, FACC and
- John Benedict, BS
- ↵*Address for reprints: Muhammad Ashraf, PhD, Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, 231 Bethesda Avenue, Cincinnati, Ohio 45267.
The effect of diltiazem, a calcium channel blocking agent, on anoxic injury was studied in isolated perfused rat hearts. Anoxia for 60 minutes caused a considerable release of creatine kinase and significant cell injury. Reoxygenation of these anoxic hearts for 20 minutes accelerated the creatine kinase release and caused severe cell injury. Reoxygenation of anoxic hearts with diltiazem at a rate of either 2 or 4.5 mg/liter did not reduce creatine kinase release significantly (probability [p] > 0.05). However, the higher dosage of diltiazem (4.5 mg/ liter during both anoxic and reoxygenation phases resulted in significant (p ≤ 0.05) preservation of healthy tissue. The data suggest that diltiazem in the higher concentration prevents cell injury and reduces mitochondrial damage in anoxic injury.
This work was supported by Research Grant HL 23597 from the National Institutes of Health, Bethesda, Maryland and Research Career Development Award K04HL00540 (Dr. Ashraf) from the U.S. Public Health Service, Bethesda, Maryland.
- Received July 15, 1982.
- Revision received October 28, 1982.
- Accepted November 5, 1982.
- American College of Cardiology Foundation