Open AccessEffects of Etafenone on Myocardial Energy Metabolism as Studied by an Organ Redoximeter and Biochemical Analyses
Author(s) -
Yasuo Etoh,
Makoto Nakazawa,
Shoichi Imai
Publication year - 1984
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.35.229
Subject(s) - creatine , adenosine triphosphate , nicotinamide adenine dinucleotide , chemistry , nad+ kinase , adenine nucleotide , high energy phosphate , ischemia , phosphate , adenosine , metabolism , phosphocreatine , biochemistry , adenosine diphosphate , oxygen , medicine , energy metabolism , nucleotide , enzyme , platelet , platelet aggregation , organic chemistry , gene
Direct recording of reduced nicotinamide adenine dinucleotide (NADH) fluorescence was conducted with an organ redoximeter in isolated perfused guinea pig heart. Cross-clamping of the aortic inflow line resulted in an increase in NADH fluorescence. After etafenone (10(-6) M), there was a significant prolongation of the time to the detectable or the maximum increase in NADH fluorescence. The magnitude of the increase in NADH fluorescence tended to be reduced (135% as compared with 145% in the control group). Supplemental chemical analyses revealed a significant increase in creatine phosphate, adenosine triphosphate (ATP) and total adenine nucleotide in the etafenone-pretreated group 15 min after postischemic reperfusion, although the ischemia-induced changes were not improved by this compound. It was suggested that the better recovery of myocardial high energy phosphate levels produced by etafenone was brought about by a decrease in oxygen consumption due to a decrease in mechanical performance of the heart and possibly by a better resynthesis of ATP.