[Protective effects of furyl-dihydropyridine I on ischemic myocardium in isolated rabbit hearts].
A recirculating nonpulsatile perfusion circuit was used in isolated rabbit hearts. Furyl-dihydropyridine I (2,6-dimethyl-4-furyl-1,4-dihydropyridine-3, 5-dicarboxylate) 20 mumol/L was shown to inhibit the release of creatine phosphokinase (CPK) and alpha-hydroxybutyrate dehydrogenase (HBD) from myocardium, decrease myocardial calcium and sodium contents by 5.3 +/- 1.1 mumol/g dry weight (P less than 0.01, n = 6) and 1.50 +/- 0.17 mmol/g dry weight (P less than 0.05, n = 6) from 8.3 +/- 1.1 mumol/g dry weight and 1.96 +/- 0.32 mmol/g dry weight respectively. It was also found to reduce coronary resistance and increase coronary flow of the ischemic myocardium, and prevent ischemic arrhythmia, thereby limit myocardial injury during regional ischemia in isolated rabbit hearts.
Liu
D Q
DQ
Department of Pharmacology, Fourth Military Medical University, Xian.
Zhao
D H
DH
Sheng
B H
BH
D000818:Animals; D002118:Calcium / Q000378:metabolism; D003326:Coronary Circulation / Q000187:drug effects*; D003327:Coronary Disease / Q000503:physiopathology; D003402:Creatine Kinase / Q000378:metabolism; D006884:Hydroxybutyrate Dehydrogenase / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D011817:Rabbits; D012964:Sodium / Q000378:metabolism; D014655:Vascular Resistance / Q000187:drug effects
D012964:Sodium; C035749:2-hydroxybutyrate dehydrogenase; D006884:Hydroxybutyrate Dehydrogenase; D003402:Creatine Kinase; D002118:Calcium