Abstract

The effect of nifedipine infusion on myocardial O2 supply and consumption in flow-restricted and normal regions of the left ventricle was tested in anaesthetized open-chest rabbits after ligation of the left anterior descending coronary artery for one hour. Ten min after occlusion, nifedipine-treated animals were given either a low or high dose of the drug: a 5 micrograms/kg bolus followed by 1 micrograms/kg per min infusion or a 10 micrograms/kg bolus and 10 micrograms/kg per min infusion, respectively. Regional blood flow was measured before and after occlusion using radioactive microspheres and O2 saturation was measured microspectrophotometrically; the Fick Principle was then employed to determine regional O2 consumption. After a 60 min occlusion, blood flow was reduced overall to 51% of pre-ligation flows in the occluded region, and treatment with nifedipine or vehicle did not significantly alter this flow reduction. Blood flow in nonoccluded regions increased 1.6-fold only with the high dose of nifedipine and was unchanged in all other groups. Microspectrophotometric analysis of low dose nifedipine and control hearts showed that O2 extraction was greater in occluded than in normal myocardium (9.0, s.d. = 0.9, ml O2/100 ml blood vs 7.2, s.d. = 0.7, respectively) and that subendocardial extraction exceeded subepicardial. These data suggest that nifedipine administration at this dose had no apparent beneficial effect on O2 supply or O2 consumption in normal or flow-restricted regions of the left ventricle during 1 h of coronary artery occlusion.

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