This study was undertaken to determine the endothelial factors involved in the flow-induced dilation of a rat perfused coronary artery. Segments of the right interventricular coronary artery were taken from 1 0-15-week-old male Wistar rats. Vessels were mounted in an arteriograph where internal diameter was continuously monitored while intraluminal pressure was controlled. Vessels were preconstricted with serotonin (10 ~tmol/L), and the dilation induced by flow (0-800 ~tl/min) was quantified. This dilator effect was measured in control conditions, after incubation with L-NAME (100 Ilmol/L), with indomethacin (100 ~tmol/L), and after mechanical destruction of the endothelium (-E). Dilations were expressed as percentage of the serotonin-induced constriction, and wall shear stress x due to the physical forces exerted on the wall of the vessel was calculated and expressed in dyn/cm 2.
In control conditions, raising the flow up to 800 I.tl/min led to an increase in dilation (maximal dilation 63%_ 4%) and in shear stress (maximal shear stress 76 +_ 4 dyn/cm2). With indomethacin, maximal dilation was 69% + 4% and maximal shear stress was 81 + 6 dyn/cm 2. With L-NAME or after destruction of endothelium, dilation was greatly reduced (39%_ 3% and 40% ± 2%, respectively) whereas shear stress values were greatly increased (173___14 and 150-t-13 dyn/cm 2, respectively).
These results confirm the viability of this model for the study of flow-dependent dilation. This dilation seems to be greatly dependent on NO release. In contrast, results do not favor a significant involvement of prostanoid vasodilating substance. Without endothelium, a dilation was still observed and showed the persistence of an endothelium-independent component of flow-induced dilation in this preparation that remains to be determined.