Abstract
The cerebral blood flow (CBF) is autoregulated to a steady flow within certain ranges. CBF increases and cerebrovascular resistance (CVR) decreases dramatically with breakthrough of autoregulation when systemic arterial blood pressure exceeded the upper limit of the range. Many kinds of components in the brain as well neurogenic factors affect the autoregulation. The breakthrough of autoregulation does not occur in the presence of nitric oxide (NO) synthesis inhibitors, angiotensin converting enzyme inhibitor, prostanoids (PG) administered in the brain, sympathetic denervation, and sinoaortic denervation. The abolishment of breakthrough of autoregulation may be due to an increased tolerance of cerebral vessels to hypertension and the inhibition of the release of a vasodilator substance such as NO or PG. It appears that the tone of brain microvessels is controlled towards dilation by cholinergic innervation originating from the nucleus basalis of Meynert, glutamatergic or GABAergic mediated GABAA receptor, and by a mediator such as NO, bradykinin, PGs. Also, it is likely that candidates for constricting factors in intraparenchymal microvessels are norepinephrinergic from the superior cervical ganglion, serotonergic involved in 5-HT1Dβ- and 5-HT2B-specific receptor subtypes, GABAergic mediated GABAB receptor, thromboxane, PG F2α and the angiotensin system. The autoregulation of CBF is maintained by these neurogenic factors to prevent brain ischemia and hyperemia.
