Background. We determined whether the coupling between cerebral blood flow
(CBF) and oxygen metabolism (CMRO2) is preserved during liver transplantati
on. Because of cerebrovascular dilatation, we hypothesized that cerebral me
tabolic autoregulation is impaired, because CBF becomes uncoupled from CMrO
(2) during the reperfusion phase of the operation.
Materials and Methods, In a prospective study, 13 patients (8 women, median
age 46, range 21-56) with liver failure (10 with end-stage chronic liver d
isease and 3 with acute liver failure) were enrolled, Catheters were placed
in a femoral artery and in the internal jugular vein for calculation of th
e cerebral arteriovenous oxygen content difference (AVDO(2)). CBF was recor
ded by the (133)Xenon injection technique, and by transcranial Doppler sono
graphy determined mean flow velocity (V-mean)in the middle cerebral artery;
The CMRO2 was calculated as the AVDO(2) times CBF and the cerebrovascular
resistance (CVR) as the mean arterial pressure to CBF ratio. An index of la
rge cerebral artery diameter was expressed by the CBF to Vmean ratio.
Results From induction of anesthesia to the anhepatic period, CBF decreased
from a median of 47 (interquartiles 31-55) to 41 (87-88) ml 100 g(-1) min(
-1), whereas the CMRO2 remained unchanghed (1.3 [0.9-2.5] vs, 1.7 [0.9-2.3]
ml 100 g(-1) min(-1)). In the reperfusion phase, the CBF increased to 51 (
45-54) ml 100 g(-1) min(-1), whereas the CMRO2 remained unchanged at 1.1 (1
.0-2.5) ml 100 g(-1) min(-1). The CVR decreased from 2.0 mm Mg (1.4-2.1) to
1.4 (1.1-1.8) mm Hg-1 min 100 g ml. In the anhepatic phase, mean arterial
pressure decreased from 92 mm Mg (84-98) to 85 (80-92) mm Mg and at reperfu
sion it was 80 (71-105) mm Mg, From the anhepatic to the reperfusion phase,
the CBF increased 7% (0 to 26) for each mpn Mg concomitant increase in Pal
CO(2),. The CBF to V-mean ratio remained stable (1.0 [0.8-1.2] vs. 0.9 [0.7
-1.1] ml 100 g(-1) min(-1) cm(-1) sec).
Conclusion. During the reperfusion phase of liver transplantations, cerebro
vascular dilatation uncouples cerebral oxidative metabolism from blood flow
. The increase in CBF is beyond what can be explained by changes in arteria
l carbon dioxide tension and arterial pressure.