AJP - Heart and Circulatory Physiology, Vol 248, Issue 4 534-H539, Copyright © 1985 by American Physiological Society
Reduction in cerebral arteriolar oxygen consumption by arachidonate
J. E. Levasseur, H. A. Kontos and E. F. Ellis
The oxygen consumption of cerebral arterioles from anesthetized cats was
measured using the Cartesian diver microrespirometer following in vitro
incubation with 200 micrograms/ml of arachidonate or 50 micrograms/ml of
15-hydroperoxy-eicosatetraenoic acid (15-HPETE). Both agents depressed
oxygen consumption severely. This effect was inhibited completely by a
combination of superoxide dismutase (SOD) and catalase, indicating that it
is mediated by oxygen radicals. Similar depression of oxygen consumption
was observed during incubation of the vessels with xanthine oxidase and
acetaldehyde as substrate. This enzymic system is known to generate
superoxide and hydrogen peroxide. The effect of xanthine oxidase was also
partially inhibited by SOD and catalase. The effect of arachidonate was
partially inhibited by cyclooxygenase inhibitors. The effect of
lipoxygenase inhibitors could not be adequately tested because they
depressed oxygen consumption by themselves. Prostaglandins H2 and E2 had no
effect on arteriolar oxygen consumption. The results show that arachidonate
and 15-HPETE in high concentration depress cerebral arteriolar oxygen
consumption via an oxygen radical-mediated mechanism. Furthermore, the
radical is generated in the vessel wall and does not require either the
brain parenchyma or the formed elements of the blood or the meninges for
its production.
