Cerebral circulation in hypoxia and XXXX .

@entity548 @entity63 @entity75 @entity26 @entity3485 @entity3209 @entity460 @entity528 @entity4095
In conclusion our results clearly suggest that vital functions of the brain, in spite of its well developed autoregulation are impaired during prolonged @entity3485 conditions. Regional cerebral blood flow measured by the 133Xe clearance and @entity3209 -antipyrine autoradiographic techniques demonstrated a progressive reduction in CBF, with the development of patchy and circumscribed @entity63 areas during @entity548 which persisted after reinfusion. The regional distribution of the underperfused regions cannot be explained solely in terms of boundary zones between the main distribution fields of major cerebral arteries. Our results suggest the involvement of the sympathetic nervous system in the impairment of cerebral microcirculation during @entity548 . The patchy focal @entity75 could be the background of the functional impairment. The focal appearances suggests that, in addition to generalized (blood borne) changes, local factors play an important role in the production of @entity63 areas in the brain. Afferent neural nociceptive input to the brain seems to be elevated during shock. It may be presumed that this leads to increased tissue metabolism and the accumulation of metabolites. The low flow combined with elevated neuronal activity and cellular metabolism produces an imbalance between @entity26 delivery and @entity26 utilization. The local nature of afferent activation of the CNS can explain the regional impairment in the brain tissue. Nociceptive afferent stimulation increases, while denervation of the carotid sinus or transsection of the vagus or spinal afferent pathways decreases the sensitivity to shock. We have presented further evidence that stimulation of the C-fibres of the sciatic nerve reduced local cerebral blood flow and the tissue @entity4095 in the n. VPL thalami and VM hypothalami in cardiovascularly restricted (stabilized blood pressure) animals. Concerning the subcellular events that may lead to @entity528 during @entity548 , we believe that the depletion of high energy phosphates initiates those complex changes which result in the loss of the viability of the affected cells. In this process the increase of free @entity460 in the cytosol probably plays a crucial role.
