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. 1987:40:95-116.
doi: 10.1007/978-3-7091-8941-2_5.

Blood flow in brain structures during increased ICP

Affiliations

Blood flow in brain structures during increased ICP

J Zierski. Acta Neurochir Suppl (Wien). 1987.

Abstract

The effect of a supratentorial expanding mass lesion and of uniform increase of ICP on regional cerebral blood flow was examined in 31 cats. The blood flow was measured using the radioactive microsphere technique and continuous ICP increase was produced by inflating an extradural balloon or by infusion of mock CSF into subarachnoid lumbar space. Four additional animals in whom no ICP rise was produced were used as controls; several blood flow measurements were performed at different ICP levels and after sudden ICP release. The analysis of the data obtained revealed that intracranial hypertension caused inhomogenous pattern of blood flow change with compartmentalization of flow between supra- and infratentorial structures connected with cisternal herniation. The flow decrease may correspond to the craniocaudal pressure gradients in the brain stem. Irrespective of the method used to produce intracranial hypertension the blood flow in the lower brain stem was less susceptible to diminished perfusion pressure. Sparing of cerebral blood flow in the lower brain stem during progressive brain compression can be explained by compartmentalization. The ranking of regions at cerebral perfusion pressure below 60 mm Hg was similar for the lower brain stem regions independently of the method which was used to increase the ICP. This suggests that when CBF becomes reduced due to increase of ICP the perfusion favours the areas where neurons related to control of circulation are located. Diffuse increase of ICP produced no interhemispheric differences in the blood flow. These differences were detected when balloon compression was used. Asymmetry of perfusion in the brain stem structures was not observed. During continuously increasing ICP an increase of blood pressure taking place before pupillary dilatation occurred was not caused by medullary ischaemia. If the pressure continued to increase the vasopressor response occurring after pupillary dilatation took place did not improve the cerebral blood flow. Increase of cerebral perfusion followed a sudden release of ICP. In an experimental animal subjected to unilateral compressive lesion producing tentorial herniation, hyperperfusion involved especially the thalamus and the midbrain with relative flow decrease in the lower brain stem.

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