Inhibition of epinephrine-exacerbated coronary thrombus formation by prostacyclin in the dog.

We studied the effect of intravenous prostacyclin (PGI2) infusion on epinephrine exacerbation of platelet-mediated acute coronary thrombus formation in an in vivo canine model of coronary artery stenosis. Platelet thrombi form in mechanically stenosed dog circumflex coronary arteries, producing cyclical reductions in coronary blood flow (CRF) as measured with an electromagnetic flowmeter probe. In the present study nine of 10 dogs exhibited spontaneously occurring CRF. With epinephrine (E) infusions of 10 micrograms/min CRF frequency increased 64% (p less than 0.025), CRF magnitude increased 27.1% (p less than 0.05), and the rate of flow decline increased 112.8%, indicating that the rate of thrombus formation increased with E infusion (p less than 0.005). When an identical E infusion was accompanied by simultaneous PGI2 infusion (150 ng/kg/min), CRF were abolished in nine of 10 dogs and markedly inhibited in the other. After the 10 min of simultaneous E and PGI2 infusion, E infusion alone was continued. There was a recurrence of CRF within 2.49 +/- 0.89 min after cessation of PGI2 infusion. However, CRF frequency in the subsequent 10 min was less than the frequency of CRF during the initial E infusion (p less than 0.10) and not significantly different from that of the control period (no E infusion). The rate of flow decline and magnitude during the final E infusion after cessation of PGI2 infusion were not significantly different from those of the initial E infusion. Prostacyclin infusion in the coronary care unit may be potentially beneficial in cases of acute myocardial ischemia where elevated catecholamines are a thrombogenic stimulus.