• P Macho and R Domenech.
• Department of Pathophysiology, Faculty of Medicine, University of Chile, Santiago, Chile.
• Can J Cardiol. 1996 Oct 1; 12 (10): 1105-9.

ObjectiveIn vitro experiments have shown that an electric field changes coronary vascular resistance (CVR) tone and damages the vascular endothelium. The effect of transthoracic electric current in dogs on the vasodilatory responses mediated through the endothelium and reactive hyperemia were studied. The manner of delivery of the electric current was similar to that used clinically during cardiac resuscitation.DesignEight mongrel dogs of either sex weighing between 15 and 22 kg were anesthetized with sodium pentobarbital. The lungs were mechanically ventilated and the thorax was opened. Circumflex coronary flow was measured with an electromagnetic flowmeter. Mean aortic pressure and the heart rate were kept constant and left ventricular systolic and diastolic pressures did not change during the procedures. The changes in CVR produced by different intracoronary doses of acetylcholine and reactive hyperemia to 10 and 30 s of circumflex coronary occlusion were measured before and after the transthoracic delivery of five synchronized electric shocks, 300 J each 1 min apart.Main ResultsCVR decreased by 32.8 +/- 2.1% (P < 0.01) from the effects of the electric shocks in spite of no changes in heart rate, ventricular systolic and diastolic pressures nor left ventricular oxygen consumption. After the delivery of the electric shocks, the vasodilatory response to acetylcholine decreased 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 coronary vascular resistance to a minimal value lower than that obtained by the maximal dose of acetylcholine but similar to before and after the passage of the electrical current revealing the preservation of the coronary vasodilatory reserve after the electrical shocks.ConclusionsThese results show that transthoracic electrical shocks as used clinically induce coronary vasodilation but simultaneously produce endothelial dysfunction.

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