Changes of collateral perfusion pressure (CPP) and segmental coronary resistances during reactive hyperemia were studied in nine chloralose-urethan-morphine anesthetized open-chest dogs. Coronary perfusion pressure was controlled by a cannula in the left main coronary artery and inflow measured by an electromagnetic flowmeter. The first or second diagonal branch of the left anterior descending coronary artery was cannulated and perfused from a carotid artery; inflow was abolished by embolization with latex microspheres (diameter: 25 +/- 5 mu) and peripheral coronary pressure was assumed to represent CPP. Segmental coronary resistances were defined as follows: Proximal coronary resistance (R1) was calculated from the difference between coronary perfusion pressure and CPP divided by coronary inflow. Distal coronary resistance (R2) was calculated from CPP divided by coronary inflow. Reactive hyperemia was produced by interruption of coronary inflow for 15 s and analysed at 30 s and 60 s of reperfusion when cardiac function had recovered. At baseline, R1 was 0.52 +/- 0.04 mm Hg X min X 100 g/ml (RU) and R2 0.63 +/- 0.07 RU. At 30 s, R1 was reduced by 19 +/- 3% (P less than 0.01) this was less (P less than 0.05) than R2 which was reduced by 32 +/- 3% (P less than 0.01). At 60 s R1 and R2 were reduced by 11 +/- 2% and 13 +/- 2%, respectively; this was not significantly different. Accordingly, CPP (baseline: 59 +/- 4 mm Hg) at 30 s was reduced by 7 +/- 2% (P less than 0.03), at 60 s the reduction was not significant. The data suggest that reactive hyperemia, as a model of metabolic coronary dilatation, may reduce CPP equivalent to a coronary steal phenomenon.