ORIGINAL ARTICLE: PDF OnlyPanagiotopoulos Sianna; Nayler, Winifred G.Journal of Cardiovascular Pharmacology: December 1987 - p 683-691 Free Abstract Summary: The excessive gain in Ca2+ that occurs when hearts are reperfused after prolonged periods of ischemia contributes to cell death and tissue necrosis. The following experiments were undertaken to determine whether nicotine, in a concentration equivalent to the peak concentration present in plasma after cigarette smoke inhalation, alters reperfusion-induced Ca2+ gain in isolated rat hearts. Nicotine (0.15 μg/ml) failed to increase tissue Ca2+ during aerobic perfusion but increased Ca2+ gain during reperfusion after 30 (p < 0.02) or 60 (p < 0.02) min of normothermic ischemia. The increase of Ca2+ gain was independent of a nicotine-induced release of norepinephrine (NE) or an altered “reflow area,‘” heart rate, force of contraction, or end-diastolic resting tension. Pretreatment for 3 days with anipamil (20 mg/kg), a long-acting calcium channel blocker, attenuated the reperfusion-induced Ca2+ gain after 30 min of global ischemia, and reduced (p < 0.001) the nicotine-induced exacerbation of that gain, without altering tissue ATP or creatine phosphate (CP). Verapamil (1 × 10−6M) reduced (p < 0.02) the nicotine-induced exacerbation of Ca2+ gain caused by reperfusion after 30 min of ischemia. © Lippincott-Raven Publishers.