RAPID CEREBRAL VASODILATATION IN BRIEF HYPOXIA IN ANAESTHETIZED ANIMALS

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Abstract
In anaesthetized dogs, cats and rabbits, intracranial pressure was measured continuously during brief or transient hypoxia, induced by (a) lowering inspired O2 to 9–10% for 2–3 min, or (b) giving 2–3 breaths of nitrogen. In almost all instances there was an increase in i.c.p. which started in less than 20 s; this occurred with either spontaneous or controlled ventilation, and whether or not there was also a rise in arterial blood pressure; the time course was similar to that of the arterial chemoreceptor reflex responses of ventilation and blood pressure. Division bilaterally of the sinus and vagus nerves in six cats showed that the intracranial pressure response was not dependent on these chemoreceptor afferent pathways. The results suggest a rapid vasodilatation starting at a time when cerebral arterial oxygen tension is unlikely to be below 7 kPa (50 mmHg). The mechanism remains unexplained.