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The goal of this study was to determine whether electrophysiological mechanisms contribute to the relaxation of cat middle cerebral artery in response to decreased ambient Po2 and whether decreased Po2 alters the myogenic depolarization and contraction of this vessel in response to elevations in transmural pressure. In one series of experiments, arterial segments (200-500 micron outer diameter) were isolated and mounted in an in vitro tension transducer to allow continuous measurement of active tension as bath Po2 was reduced. In these experiments, vessel relaxation occurred primarily between 150 mm Hg Po2 and 40 mm Hg Po2, suggesting that cerebral arteries are sensitive to alterations of Po2 in the physiological range. Relaxation did not result from the activation of dilator nerves in the vessel wall, since it was unaffected by tetrodotoxin. Arterial segments were also cannulated with micropipettes and subjected to elevations in transmural pressure during 300 mm Hg Po2 and 50 mm Hg Po2 superfusion. During 300 mm Hg Po2 superfusion, cannulated vessels exhibited myogenic depolarization and maintained their diameter as transmural pressure was increased; 50 mm Hg Po2 superfusion inhibited spontaneous spike activity, decreased the slope of the myogenic depolarization, and partially inhibited vessel contraction in response to elevated transmural pressure. These effects are independent of the parenchymal cell environment and appear to be mediated, at least in part, by electrophysiological mechanisms.

Effect of reduced oxygen availability upon myogenic depolarization and contraction of cat middle cerebral artery.