Starnes V A, Primm R K, Woosley R L, Oates J A, Hammon J W
J Cardiovasc Pharmacol. 1982 Sep-Oct;4(5):765-9. doi: 10.1097/00005344-198209000-00011.
The effects of prostacyclin (PGI2) on ventricular arrhythmias following 20 min of coronary occlusion and release were studied in 34 conscious dogs. We administered PGI2 at 100 ng/kg/min and did not observe significant changes in heart rate, blood pressure, or systemic vascular resistance. During the control period, heart rate was 97 +/- 30 (mean +/- SEM) vs. 99 +/- 28 in the PGI2-treated group. Mean arterial pressure was 115 +/- 26 mm Hg and 109 +/- 10 mm Hg in the control and PGI2 groups, respectively. Systemic vascular resistance declined minimally from 2,985 +/- 221 dyn . s . cm-5 to 2,484 +/- 135 dyn . s . cm-5 during the PGI2 infusion (p = NS). Following coronary occlusion, the frequency of ventricular fibrillation was reduced from 53% (9/17) in the control group to 6% (1/17) in the PGI2 group (p less than 0.01). Overall 80-min postinfarction survival was 64% in the group receiving PGI2 infusion compared to 24% in the control group (p less than 0.05). The effects of PGI2 in preventing ventricular fibrillation following acute coronary occlusion can be ascribed to a direct action of this prostaglandin on the myocardium, rather than to an indirect effect due to a reduction in systemic vascular resistance.
