Abstract

Excessive cigarette smoking acts synergistically with atheromatous coronary artery disease to greatly enhance the risk of acute myocardial infarction. To explore a possible mechanism of this relation, the present study tested the hypotheses that diet-induced atherosclerosis in rabbits is associated with an increase in myocardial (−)-norepinephrine content and that the increased (−)-norepinephrine can be released by nicotine. Adult male rabbits were rendered atherosclerotic by feeding them a standard laboratory diet enriched with 2% cholesterol. After 12–13 weeks on the diet, hearts were excised and retroperfused according to the Langendorff technique. There were no differences between control and atherosclerotic animals in terms of baseline (−)-norepinephrine concentration in the coronary effluent. However, increases in effluent (−)-norepinephrine concentration provoked by 10 μg and 30 μg nicotine were significantly greater in atherosclerotic hearts than in controls. Similarly, myocardial tissue from atherosclerotic animals contained significantly more (−)-norepinephrine than controls. These observations suggest that diet-induced atherosclerosis in rabbits is associated with an increase in myocardial (−)-norepinephrine content and that the augmented (−)-norepinephrine pool can be mobilized by nicotine.

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