The observed positive correlation between cessation of red blood cell flow in capillaries at low perfusion pressures and the oxygen tension (PO2) in the superfusion solution may be due to oxygen-dependent arteriolar constriction. To test this hypothesis, we investigated capillary flow cessation during aortic occlusion and concomitant changes in diameters of terminal arterioles and capillaries in normal and vasodilated vascular beds of rabbit tenuissimus muscle (n = 15) by means of video intravital microscopy. In the vasodilated bed, arteriolar tone was eliminated by local application of 10-4M adenosine (ADO). The PO2 in the superfusate was varied locally, i.e., in the solution between objective lens and muscle surface. At a local PO2 of 40 mm Hg without ADO, flow ceased in about 50% of the capillaries during aortic occlusion while the arterioles dilated to 118% of control (median; p < 0.001). Addition of ADO led to an increase in arteriolar and capillary diameter to 220% (median; p < 0.001) and 121% (median; p < 0.05), respectively. Under ADO, the incidence of capillary flow cessation was reduced (p < 0.05) to about 20%. Elevation of the local PO2 from 40 to 100 mm Hg in the presence of ADO did not lead to a significant change in the incidence of flow cessation, nor to changes in arteriolar or capillary diameter. In the presence of ADO, median arteriolar and capillary diameters during aortic occlusion were 96% (p < 0.001) and 7% (p < 0.05) larger than their control diameters without ADO, respectively. In summary, it is suggested that the incidence of flow cessation may depend on both the arteriolar and the capillary diameter. Of these two factors, capillary diameter may be the most important one, because its changes affect the interaction between red blood cells and the vessel wall in the narrow capillaries, and, hence, the resistance to flow. In the presence of ADO, at elevated local PO2 levels flow cessation still occurs in about 20-30% of the capillaries, suggesting that arteriolar contraction is only in part responsible for the incidence of flow cessation.