Prevention of global myocardial reperfusion injury on isolated rabbit hearts with furyl-dihydropyridines I.
In the isolated rabbit heart of recirculating nonpulsatile perfusion circuit, furyl-dihydropyridines I 20 mumol.L-1 greatly reduced the leakage of myocardial enzymes and the concentration of malondialdehyde (MDA) in plasma, decreased the myocardial calcium and sodium contents, maintained normal coronary vascular resistance and prevented reperfusion arrhythmias of global postischemic reperfusion hearts. Its mechanism of protecting the ischemic-reperfused myocardium might be associated with the diminution of calcium influx of myocardial cells and cellular lipid peroxidation induced by oxygen free radicals.
Liu
D Q
DQ
Department of Pharmacology, Fourth Military Medical University, Xi-an, China.
Zhao
D H
DH
Sheng
B H
BH
D000818:Animals; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D003402:Creatine Kinase / Q000097:blood; D004095:Dihydropyridines / Q000494:pharmacology*; D006884:Hydroxybutyrate Dehydrogenase / Q000097:blood; D066298:In Vitro Techniques; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism; D011817:Rabbits; D012964:Sodium / Q000378:metabolism; D014655:Vascular Resistance / Q000187:drug effects
D002121:Calcium Channel Blockers; D004095:Dihydropyridines; C071424:2,6-dimethyl-4-furyl-1,4-dihydropyridine-5-dicarboxylate; D008315:Malondialdehyde; D012964:Sodium; C035749:2-hydroxybutyrate dehydrogenase; D006884:Hydroxybutyrate Dehydrogenase; D003402:Creatine Kinase; D002118:Calcium