TY - JOUR
T1 - Effects of diltiazem on anoxic injury in the isolated rat heart
AU - Rahamathulla, Pacha Meyian
AU - Ashraf, Muhammad
AU - Schwartz, Arnold
AU - Benedict, John
N1 - Funding Information:
From the Department of Pathology and Laboratory Medicine and the Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Cincinnati, Ohio. This work was supported by Research Grant HL 23597 from the National Institutes of Health, Bethesda, Maryland and Research Career Development Award K04HLOO540 (Dr. Ashraf) from the U.S. Public Health Service, Bethesda, Maryland. Manuscript received July 15, 1982; revised manuscript received October 28, 1982, accepted November 5, 1982. Address for reprints: Muhammad Ashraf, PhD, Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, 231 Bethesda Avenue, Cincinnati, Ohio 45267.
PY - 1983
Y1 - 1983
N2 - 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.
AB - 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.
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U2 - 10.1016/S0735-1097(83)80110-7
DO - 10.1016/S0735-1097(83)80110-7
M3 - Article
C2 - 6833646
AN - SCOPUS:0020566007
SN - 0735-1097
VL - 1
SP - 1081
EP - 1089
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 4
ER -