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REGIONAL O 2 SUPPLY/CONSUMPTION IN NORMAL AND ISCHAEMIC RABBIT MYOCARDIUM: EFFECT OF NIFEDIPINE
Author(s) -
Eliades Diane,
Talafih Khalid,
Weiss Harvey R.
Publication year - 1985
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1985.tb00880.x
Subject(s) - nifedipine , ventricle , blood flow , occlusion , bolus (digestion) , ligation , anesthesia , medicine , chemistry , cardiology , calcium
SUMMARY 1. The effect of nifedipine infusion on myocardial O 2 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. 2. Ten min after occlusion, nifedipine‐treated animals were given either a low or high dose of the drug: a 5 μg/kg bolus followed by 1 μg/kg per min infusion or a 10 μg/kg bolus and 10 μg/kg per min infusion, respectively. Regional blood flow was measured before and after occlusion using radioactive microspheres and O 2 saturation was measured microspectrophotometrically; the Fick Principle was then employed to determine regional O 2 consumption. 3. 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. 4. Blood flow in nonoccluded regions increased 1.6‐fold only with the high dose of nifedipine and was unchanged in all other groups. 5. Microspectrophotometric analysis of low dose nifedipine and control hearts showed that O 2 extraction was greater in occluded than in normal myocardium (9.0, s.d. = 0.9, ml O 2 /100 ml blood vs 7.2, s.d. = 0.7, respectively) and that subendocardial extraction exceeded subepicardial. 6. These data suggest that nifedipine administration at this dose had no apparent beneficial effect on O 2 supply or O 2 consumption in normal or flow‐restricted regions of the left ventricle during 1 h of coronary artery occlusion.