Despite the numerous studies examining the relative merits of crystalloids versus colloids for expansion of intravascular volume, little attention has been directed to the cerebral effects of these solutions. In particular, the effect of changes in plasma oncotic pressure on brain water content are poorly understood. The authors recently examined the acute effects of changes in plasma osmolality and colloid oncotic pressure in normal animals, and found that a 65% reduction in oncotic pressure had no detectable effect on brain water content or intracranial pressure. In an effort to extend these studies to a more clinically relevant situation, the authors have now compared the acute effects of 0.9% saline, 6% hetastarch, and 5% albumin on regional cerebral water content and intracranial pressure in an animal model of brain injury produced by focal cortical freezing. Under general anesthesia and following the production of the cryogenic brain lesion, rabbits underwent a 45-min period of isovolemic hemodilution to a hematocrit of 20-25% with one of the three selected fluids. The saline group required approximately twice as much fluid (207 +/- 17 ml) to maintain a stable mean arterial pressure and central venous pressure as did the hetastarch (105 +/- 14 ml) or albumin (103 +/- 29 ml) groups. As intended, the oncotic pressure decreased by a mean of 9.6 +/- 2.4 mmHg in the saline group, while remaining stable in the hetastarch and albumin groups. There were no significant changes in osmolality in any group during the hemodilution period. Intracranial pressure increased in all groups following production of the cerebral lesion, but there were no differences between the various experimental groups upon conclusion of the hemodilution. Brain water content was significantly increased in the vicinity of the cryogenic lesion, but there were no differences between the various hemodilution groups. This experimental suggests that a decrease in plasma oncotic pressure due to the administration of an isotonic crystalloid solution does not acutely exacerbate the cerebral edema that is produced by this model of brain injury.
(C) 1988 American Society of Anesthesiologists, Inc.