Effects of nifedipine on creatine kinase release during myocardial ischemia in dogs.

25 anesthetized mongrel dogs underwent a left thoracotomy. Creatine kinase (CK) activity was measured in serial blood samples drawn simultaneously from the aorta and a coronary vein. The distribution of myocardial perfusion was determined by a continuous infusion of krypton-81m (half-life 13 sec) into the aortic sinuses. Heart rate and arterial blood pressure were also measured throughout the procedure. In 20 dogs regional myocardial ischemia was produced by ligation of a major branch of the left anterior descending coronary artery. Five of these dogs received 1 microgram.kg-1 nifedipine i.v. and a further 5 received 13 microgram.kg-1. Thoracotomy alone produced a slight rise in plasma CK activity but the arteriovenous difference (AV) across the segment of the heart remained positive over 5 h. Myocardial ischemia in the untreated dogs caused a considerable increase in CK activity and the AV difference became negative at 90 min. Treatment with the lower dose of nifedipine considerably reduced the plasma CK activity and the AV difference did not become negative until 3 h. Regional myocardial perfusion showed a significant improvement. Conversely, the higher dose of nifedipine produced a marked increase in the area of ischemia and an acceleration of CK release from the heart. This was associated with a decrease in arterial pressure and an increase in heart rate. These results show that nifedipine can be beneficial in experimental myocardial infarction but care must be taken to avoid hypotension and increases in heart rate.