Ms. Houle et al., Enhanced in vivo and in vitro contractile responses to beta(2)-adrenergic receptor stimulation in dogs susceptible to lethal arrhythmias, J APP PHYSL, 91(4), 2001, pp. 1627-1637
The response to beta -adrenergic receptor (beta -AR) stimulation was evalua
ted in both isolated cardiomyocytes (video edge detection) and the intact a
nimal (echocardiography) in dogs either susceptible (S) or resistant (R) to
ventricular fibrillation induced by a 2-min coronary occlusion during the
last minute of exercise. In the intact animal, velocity of circumferential
fiber shortening (Vcf) was evaluated both before (n = 27, S = 12 and R = 15
) and after myocardial infarction. Before infarction, increasing doses of i
soproterenol provoked similar contractile and heart rate responses in each
group of dogs. Either beta (1)-AR (bisoprolol) or beta (2)-AR (ICI-118551)
antagonists reduced the isoproterenol response, with a larger reduction not
ed after the beta (1)-AR blockade. In contrast, after infarction, isoproter
enol induced a significantly larger Vcf and heart rate response in the susc
eptible animals that was eliminated by beta (2)-AR blockade. The single-cel
l isotonic shortening response to isoproterenol (100 nM) was also larger in
cells obtained from susceptible compared with resistant dogs and was reduc
ed to a greater extent by beta (2)-AR blockade in the susceptible dog myocy
tes (S, - 48%, n = 6; R, - 15%, n = 9). When considered together, these dat
a suggest that myocardial infarction provoked an enhanced beta (2)-AR respo
nse in susceptible, but not resistant, animals.