P. Macho et R. Domenech, EFFECT OF TRANSTHORACIC ELECTRIC-CURRENT ON THE CORONARY CIRCULATION OF THE DOG, Canadian journal of cardiology, 12(10), 1996, pp. 1105-1109
OBJECTIVE: In vitro experiments have shown that an electric field chan
ges coronary vascular resistance (CVR) tone and damages the vascular e
ndothelium. The effect of transthoracic electric current in dogs on th
e vasodilatory responses mediated through the endothelium and reactive
hyperemia were studied. The manner of delivery of the electric curren
t was similar to that used clinically during cardiac resuscitation. DE
SIGN: Eight mongrel dogs of either sex weighing between 15 and 22 kg w
ere anesthetized with sodium pentobarbital. The lungs were mechanicall
y ventilated and the thorax was opened. Circumflex coronary flow was m
easured with an electromagnetic flowmeter. Mean aortic pressure and th
e heart rate were kept constant and left ventricular systolic and dias
tolic pressures did not: change during the procedures. The changes in
CVR produced by different intracoronary doses of acetylcholine and rea
ctive hyperemia to 10 and 30 s of circumflex coronary occlusion were m
easured before and after the transthoracic delivery of five synchroniz
ed electric shocks, 300 J each 1 min apart. MAIN RESULTS: CVR decrease
d by 32.8+/-2.1% (P<0.01) from the effects of the electric shocks in s
pite of no changes in heart rate, ventricular systolic and diastolic p
ressures nor left ventricular oxygen consumption. After the delivery o
f the electric shocks, the vasodilatory response to acetylcholine decr
eased by a mean value of 35.9+/-2.6% for the different doses (P<0.001)
and reactive hyperemia decreased by 42.5+/-5.5% (P<0.001) and by 31.5
+/-9.6% (P<0.02) for the 10 and 30 s occlusion duration, respectively.
The intracoronary infusion of sodium nitroprusside decreased the coro
nary vascular resistance to a minimal value lower than that obtained b
y the maximal dose of acetylcholine but similar to before and after th
e passage of the electrical current revealing the preservation of the
coronary vasodilatory reserve after the electrical shocks. CONCLUSIONS
: These results show that transthoracic electrical shocks as used clin
ically induce coronary vasodilation but simultaneously produce endothe
lial dysfunction.