Effect of carbon monoxide on rabbit cerebral arteries

Carbon monoxide produces relaxation in some peripheral arteries. Recently it has been suggested that carbon monoxide may be generated in brain tissue. In the present study we examined the hypothesis that carbon monoxide directly relaxes cerebral blood vessels.

The aorta and basilar and middle cerebral arteries were removed from New Zealand White rabbits and mounted for tension recording in vitro. Canine basilar arteries were also studied. After precontraction, cumulative relaxation concentration-response curves to carbon monoxide, nitric oxide, sodium nitroprusside, acetylcholine (rabbit arteries), and ATP (dog basilar artery) were obtained. Maximum relaxation and the concentration of agonists that induced half-maximal relaxation (ED50) were determined.

Carbon monoxide (10(-6) to 3 x 10(-4) mol/L) did not affect tension in rabbit or dog cerebral arteries. In rabbit aorta, carbon monoxide induced 29 +/- 4% (mean +/- SEM) relaxation at the highest concentration used (3 x 10(-4) mol/L). In contrast, nitric oxide produced 80% to 100% relaxation of all arteries, with ED50 values ranging from 7.1 to 7.4 -log mol/L. Nitroprusside, acetylcholine, and ATP also produced 80% to 100% relaxation of the arteries.

Carbon monoxide does not appear to have significant effect on tone in cerebral arteries. In contrast, at high concentrations carbon monoxide produces concentration-dependent relaxation in rabbit aorta. Factors that account for this regional heterogeneity are not clear. Although neurons may produce both nitric oxide and carbon monoxide, our findings suggest that only nitric oxide has direct effects on cerebral vascular tone.