Effects of α-adrenergic blockade on coronary autoregulation in dogs

In α-chloralose-anesthetized, open-chest dogs, left coronary blood flow and oxygen extraction were measured at perfusion pressures from 25 to 175 mmHg. Pressure-flow relationships were obtained before and after α-blockade with prazosin or α₂-blockade with yohimbine in the presence of β-blockade with propranolol. The efficiency of flow autoregulation with increments in pressure was calculated as the closed-loop gain and as the slope of flow to pressure. In all animals the highest gain and the lowest slope were seen when pressure increased from 75 to 125 mmHg. In the prazosin group before α-blockade the gain with this pressure increase was 0.76 ± 0.05, whereas in the yohimbine group before α-blockade this gain was 0.75 ± 0.03. Prazosin reduced the gain within the pressure range of 75-125 mmHg by 41%, and this reduction was statistically significant (P < 0.05). Prazosin also significantly increased the flow to pressure slope within this range. In addition, at all pressures ≥50 mmHg, the level of coronary flow was significantly increased by prazosin. The increase in flow and the reduction in autoregulatory efficiency with prazosin were not attributable to an increase in myocardial oxygen consumption. Yohimbine had no effects on the level of coronary flow or on the autoregulatory efficiency. These data indicate that an α₁-adrenoceptor mediated coronary constriction modulates coronary autoregulation.