Effects of diltiazem on anoxic injury in the isolated rat heart

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 ki...

Full description

Saved in:
Bibliographic Details
Published in:Journal of the American College of Cardiology 1983-04, Vol.1 (4), p.1081-1089
Main Authors: Rahamathulla, Pacha Meyian, Ashraf, Muhammad, Schwartz, Arnold, Benedict, John
Format: Article
Language:English
Subjects:
Aerobiosis
Animals
Benzazepines - pharmacology
Creatine Kinase - metabolism
Diltiazem - pharmacology
Diltiazem - therapeutic use
Dose-Response Relationship, Drug
Heart - drug effects
Hypoxia - complications
Hypoxia - drug therapy
Hypoxia - pathology
Male
Mitochondria, Heart - ultrastructure
Myocardium - metabolism
Myocardium - ultrastructure
Oxygen Consumption
Perfusion
Rats
Rats, Inbred Strains
Space life sciences
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:0735-1097
1558-3597
DOI:10.1016/S0735-1097(83)80110-7