Effect of Nicotine on Severity of Acute Myocardial Ischemic Injury in Dogs

Abstract

This study was undertaken to examine the effect of nicotine intravenously (i.v.) on the severity of myocardial ischemic injury following acute coronary artery occlusion in dogs. The myocardial ischemic area was measured by the sum of ST-segment elevations (ST) in epicardial ECG-registrations from 5–12 sites in nine anesthetized open-chest dogs. During coronary artery occlusion alone, ST averaged 22.7 ± 4.6 mV (mean ± S.E.M.). At reocclusion of the coronary artery during a continuous i.v. infusion of nicotine, ∑ ST rose by 6.4 ± 1.8 mV (P < 0.01). Arterial concentration of free fatty acids (FFA) rose from 251 ± 31 μEq/l to 323 ± 50 μEq/l (P < 0.05). When lipolysis was inhibited with β-pyridyl carbinol, as examined in six dogs, nicotine i.v. failed to raise ∑ ST at coronary occlusion, nor did arterial concentration of FFA rise. In conclusion the increased severity of acute myocardial ischemic injury induced by nicotine is probably related in increased myocardial oxygen requirements caused by excess myocardial consumption of FFA.

Key Words:

• β-pyridyl carbinol
• coronary occlusion
• epicardial ECG
• free fatty acids
• lipolysis
• myocardial ischemia
• nicotine
• ST-segment elevation