Y. Birnbaum et al., IS PRECONDITIONING BY NICOTINE RESPONSIBLE FOR THE BETTER PROGNOSIS IN SMOKERS WITH ACUTE MYOCARDIAL-INFARCTION, Basic research in cardiology, 91(3), 1996, pp. 240-247
Cigarette smoking is a well-known risk factor for acute myocardial inf
arction and sudden death. However, a history of smoking consistently h
as been associated with better hospital outcome in patients with acute
myocardial infarction. The mechanism for the better outcome in smoker
s is not clear. It has been suggested that nicotine may have a ''preco
nditioning-like'' effect. This study assesses whether nicotine attenua
tes myocardial infarct size. Anesthetized rabbits were randomized to r
eceive infusion of nicotine 80 mu g/kg (n = 13), or saline (n = 12) ov
er 10 min. Twenty minutes after termination of infusion all rabbits un
derwent 30 min of coronary artery occlusion and 4 h of reperfusion. Ri
sk zone was assessed by blue dye and infarct size by tetrazolium stain
ing. Nicotine did not affect regional myocardial blood flow 15 min aft
er treatment, during occlusion or during reperfusion. Heart rate and m
ean systemic blood pressure were similar between the groups. Nicotine
serum levels during occlusion were 9.5-22.0 ng/ml in the treated group
, which are comparable to levels found in human smokers. No difference
s were found in the risk zone of nicotine compared to control rabbits
(26 +/- 2% vs. 23 +/- 2% of the left ventricle, respectively). or infa
rct size (31 +/- 5% vs. 37 +/- 4% of risk zone). Since no effect on in
farct size was found, a third group receiving higher dose of nicotine,
320 mu g/kg (n = 6), was added. Infarct size was not different from t
he control group (39 +/- 6% of risk zone). Nicotine, given intravenous
ly before ischemic insult, does not protect the myocardium. A ''precon
ditioning-like'' effect of nicotine is probably not the mechanism of r
educed mortality in smoking patients with myocardial infarction.