Effects of alterations in arterial CO2 tension on cerebral blood flow during acute intracranial hypertension in rats

Cerebrovascular reactivity to CO2 in clinical and experimental studies has been found to be impaired during increased intracranial pressure (ICP). How ever, from previous study results it has not been possible to estimate whet her the impairment was caused by elevated ICP, or caused by decreased cereb ral perfusion pressure (CPP). The current study was carried out in a group of unmanipulated control rats and in six investigation groups of six rats e ach: two groups with elevated ICP (30 and 50 mm Hg) and spontaneous arteria l blood pressure (MABP), two groups with spontaneous ICP and arterial hypot ension (77 and 64 mm Hg), and two groups with elevated ICP (30 and 50 mm HE ) and arterial hypertension (124 mm Hg). Intracranial hypertension was indu ced by continuous infusion of lactated Ringer's solution into the cisterna magna, arterial hypotension by controlled bleeding, and arterial hypertensi on by continuous administration of norepinephrine intravenously. Cerebral b lood flow (CBF) was measured repetitively by the intraarterial Xe-133 metho d at different levels of arterial PCO2. In each individual animal, CO2 reac tivity was calculated from an exponential regression line obtained from the corresponding CBF/PaCO2 values. By plotting each individual value of CO2 r eactivity against the corresponding CPP value from the seven investigation groups, CPP was significantly and directly related to CO2 reactivity of CBF (P < .001). No correlation was found by plotting CO2 reactivity values aga inst the corresponding MABP values or the corresponding ICP values. Thus, t he results show that CO2 reactivity is at least partially determined by CPP and that the impaired CO2 reactivity observed at intracranial hypertension and arterial hypotension may be caused by reduced CPP.