Autoregulation of Cerebral Blood Flow

Abstract

Autoregulation is a result of an intrinsic character of vascular smooth muscle cells. Other factors interact with pressure to define the degree of contraction of the smooth muscle cell. The final common pathway involves plasma membrane potassium conductance, smooth cell membrane potential, and cytoplasmatic calcium concentration. The molecular mechanisms are too complex to allow quantitative predictions. Autoregulation operates in most newborn infants (even the most immature), although the cerebral blood flow (CBF)-pressure relation is not likely to be strictly flat. In severely asphyxiated neonates, in preterm neonates who eventually develop major intracranial hemorrhage, and in hypotensive preterm infants treated with dopamine, the CBF-pressure relation is significantly above zero and may be as high as 4% per millimeter of mercury, corresponding to complete pressure passiveness. The lower threshold for cerebral autoregulation can be assumed to be 30 mm Hg or below. When blood pressure falls below this threshold, CBF decreases more than in proportion to pressure due to the elastic reduction in vascular diameter, but significant blood flow can be assumed to continue until the blood pressure is well below 20 mm Hg. The clinical relevance of autoregulation of CBF is the ability of cerebral arteries and arterioles to dilate to compensate for low blood pressure and protect against ischemic brain injury. The importance of the ability to constrict to protect against cerebral hemorrhage is not supported by clinical research.