RT Journal
A1 Greenspan K, Edmands RE, Knoebel SB, Fisch C
T1 SOme effects of nicotine on cardiac automaticity, conduction, and inotropy
JF Archives of Internal Medicine
JO Archives of Internal Medicine
YR 1969
FD June 1
VO 123
IS 6
SP 707
OP 712
DO 10.1001/archinte.1969.00300160097016
UL http://dx.doi.org/10.1001/archinte.1969.00300160097016
AB The actions of nicotine upon the heart are numerous and varied, affecting rate,1 contractile force,1-3 and, in all likelihood, coronary flow.4 It is generally considered that a large proportion of this alkaloid's cardiovascular affects are mediated via the autonomic nervous system1 in accordance with nicotine's well-established 1 capacity to stimulate, then paralyze all autonomic ganglia. In the case of the heart, then, this drug initially produces cardiac slowing as a consequence of vagal stimulation. Subsequently, with paralysis of the vagal ganglia, there characteristically occurs an acceleration of heart rate, associated with release of cardiac stores of catecholamines.The characteristic enhancement of contractile force following nicotine administration has previously 1 been attributed to the above-described release of catecholamines. More recent studies3 have demonstrated, however, that higher concentrations of the alkaloid produce a positive inotropic effect upon isolated cat papillary muscle and that the effect is unrelated