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Effect of atrial natriuretic peptide on electrical defibrillation efficacy
Y Murakawa1, T Yamashita, Y Kanese
1Second Department of Internal Medicine, University of Tokyo, Japan. murakawa-2im@h.u-tokyo.ac.jp
Introduction:
In vitro studies have suggested that human atrial natriuretic peptide (ANP) modulates the electrophysiologic properties of myocardial cells. This study assessed whether ANP could influence defibrillation efficacy.
Methods And Results:
In 35 anesthetized dogs, the transcardiac defibrillation threshold (DFT) as well as hemodynamic and electrophysiologic variables were determined before and during treatment with ANP (n = 11), hydralazine (n = 11), or saline (n = 13). ANP (1.5 microg/kg + 0.2 microg/kg per min) increased the plasma concentration of cyclic GMP (a second messenger for ANP) and significantly decreased aortic blood pressure (mean 100+/-11 mmHg to 83+/-15 mmHg). ANP also prolonged ventricular repolarization (effective refractory period 157+/-7 msec to 165+/-11 msec) and markedly reduced DFT (5.4+/-1.2 J to 3.8+/-0.7 J [P < 0.01]) without changing pulmonary artery pressure or sinus cycle length. Neither saline nor hydralazine (1.5 mg/kg) had a significant effect on DFT (saline 4.7+/-2.1 J to 4.6+/-2.4 J; hydralazine 4.3+/-2.0 J to 4.2+/-1.9 J), although hydralazine caused pronounced hypotension (mean aortic pressure 103+/-9 mmHg to 74+/-13 mmHg).
Conclusion:
These results suggest that ANP increases defibrillation efficacy, and that this effect is not necessarily shared by other vasodilating agents.