Effects of dilazep in evolving myocardial infarction in dogs: a biochemical study

Mongrel dogs of either sex with ligation of their left anterior descending coronary artery were employed for the present study to investigate the biochemical basis of the cardioprotective action of dilazep. Dilazep (0.2 mg/kg intravenous) was administered 20 minutes after coronary arterial occlusion. Ligation of the artery for 40 minutes increased the tissue lactate concentration and decreased the adenosine triphosphate molecules within the occluded bed. Dilazep decreased the lactate concentration and improved the adenosine triphosphate content of this bed significantly. Dilazep also lowered the tissue cyclic adenosine monophosphate concentration and free fatty acid extraction of the ischemic myocardium as studied 40 minutes after coronary arterial ligation. It can be inferred that less free fatty acid extraction and calcium antagonistic action of dilazep helps in restoring mitochondrial function. Furthermore, decreased tissue lactate concentration resulted after better perfusion of the occluded bed and helped in greater generation of adenosine triphosphate molecules. These favorable biochemical and metabolic changes contribute to the cardioprotective action of dilazep.