EFFECT OF TRANSTHORACIC ELECTRIC-CURRENT ON THE CORONARY CIRCULATION OF THE DOG

Citation
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
Citations number
20
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
0828282X
Volume
12
Issue
10
Year of publication
1996
Pages
1105 - 1109
Database
ISI
SICI code
0828-282X(1996)12:10<1105:EOTEOT>2.0.ZU;2-T
Abstract
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.