Changes in the rate of formation and resistance to reabsorption of cerebrospinal fluid during deliberate hypotension induced with adenosine or hemorrhage

Adenosine is recommended for induction of deliberate hypotension. Although its effects on brain vasculature and metabolism and intracranial pressure have been reported, its effects on cerebrospinal fluid dynamics have not. In this study the rate of cerebrospinal fluid formation (V(f)), resistance to reabsorption of cerebrospinal fluid (R(a)), and electroencephalogram (EEG) activity were determined in rabbits before and during decrease of cerebral perfusion pressure (CPP) with intravenous (iv) adenosine or hemorrhage. In the adenosine group (n = 6), V(f) and R(a) were determined at control CPP, at CPP of 50, 35, and 28 mmHg achieved with iv adenosine, and at CPP > 60 mmHg achieved with iv adenosine combined with iv phenylephrine. In the hemorrhage group (n = 6), V(f) and R(a) were determined at the first four experimental conditions only. Control values for V(f) (9 ± 3 and 9 ± 4 μl·min^-1, mean ± SD) and R(a) (428 ± 567 and 412 ± 144 cmH₂O·ml^-1·min) did not differ between groups. In the adenosine group, V(f) did not change significantly when CPP was decreased. However, in the hemorrhage group, V(f) decreased significantly at CPP of 50 and 35 mmHg and became unmeasurable at CPP of 28 mmHg. R(a) did not change significantly in either group. An increase of low-frequency (0.5-3.0 Hz) EEG activity and/or decrease of higher-frequency (3.5-30 Hz) EEG activity occurred at CPP of 28 mmHg in the adenosine group and at CPP of 35 mmHg in the hemorrhage group. It is concluded that V(f) is preserved during adenosine-induced hypotension, presumably because of the dilating action of adenosine on the vasculature of the choroid plexus, and that V(f) decreases during hemorrhagic hypotension, presumably because of the vasoconstrictor response to hemorrhage.