Cerebrovascular response to intracranial hypertension

Pial arterial and venous calibre changes during intracranial hypertension were studied in 11 cats under barbiturate- and nitrous oxide-anaesthesia by using a closed cranial window technique and multichannel videoangiometry. Intracranial pressure was elevated from a normal mean level of 6.4 mm Hg by cisternal infusion of mock CSF in steps to 20, 30, 40, 50 mm Hg and finally to the level of systolic pressure. Pial arteries dilated significantly, small ones more than large ones, by 42 +/- 5.6% and 33 +/- 3%, respectively at ICP 50. With a further elevation of ICP up to systolic pressure, dilatation diminished to 28 +/- 10% in small, and to near resting calibres in large arteries. Pial veins remained unreactive on the average. Grouping into veins smaller and larger than 100 microns of resting size revealed, however, minor though statistically significant 5-10% dilatation of small, and a 5-10% diminution of large veins. Blood flow stopped, when cerebral perfusion pressure was zero, however, neither arteries nor veins collapsed. The present data support the hypothesis that CBF during acute elevation of CSF pressure depends on perfusion pressure rather than local vascular compression.