The effect of bilirubin on vasoreactivity was examined in the exposed rabbit basilar artery (diameter, 1045 +/- 17-mu-m; n = 18) and its cortical branches (diameter, 265 +/- 11-mu-m; n = 43) in vivo. Vasoconstriction induced by uridine triphosphate (UTP; 10(-5) to 10(-3) mol/L) was observed in vivo before and after a 60-minute application of supersaturated bilirubin (10(-4) mol/L). Bilirubin was dissolved in modified artificial cerebrospinal fluid (pH 7.4) or in physiological salt solution (pH 7.6). The latter was spectrophotometrically estimated to contain a higher concentration of free bilirubin because of the formation of less colloid. After treatment with bilirubin in artificial cerebrospinal fluid, the effect was minimal in the basilar arteries (n = 7), whereas the diameter of the branches was reduced by 9.6 +/- 1.5% (n = 23) and UTP-induced vasoconstriction was potentiated. After application of bilirubin in physiological salt solution, the basilar arteries contracted slightly (-2.1 +/- 0.9%; n = 6) and the UTP-induced vasoconstriction in the branches was attenuated (n = 12). After a 60-minute incubation of basilar artery with bilirubin in physiological salt solution in vitro, isometric tension recordings showed a diminution in KCl- and UTP-induced vasoconstrictions. Acetylcholine- and sodium nitroprusside-induced relaxations were also attenuated. It is suggested that bilirubin may exert different effects depending on the size of arteries and the concentration of free bilirubin. The constrictor and potentiating effects of bilirubin could be caused by the impairment of the relaxation mechanism. When the toxic effect of bilirubin becomes severe, the constrictor mechanism is also damaged.
