Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1081-1089 |
| Number of pages | 9 |
| Journal | Journal of the American College of Cardiology |
| Volume | 1 |
| Issue number | 4 |
| DOIs | |
| State | Published - Jan 1 1983 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
Effects of diltiazem on anoxic injury in the isolated rat heart. / Rahamathulla, Pacha Meyian; Ashraf, Muhammad; Schwartz, Arnold; Benedict, John.
In: Journal of the American College of Cardiology, Vol. 1, No. 4, 01.01.1983, p. 1081-1089.Research output: Contribution to journal › Article
}
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
PY - 1983/1/1
Y1 - 1983/1/1
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.
UR - http://www.scopus.com/inward/record.url?scp=0020566007&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0020566007&partnerID=8YFLogxK
U2 - 10.1016/S0735-1097(83)80110-7
DO - 10.1016/S0735-1097(83)80110-7
M3 - Article
C2 - 6833646
AN - SCOPUS:0020566007
VL - 1
SP - 1081
EP - 1089
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
SN - 0735-1097
IS - 4
ER -