Metabolic effects of a late hypotensive insult combined with reduced intracranial compliance following traumatic brain injury in the rat.
BACKGROUND
Traumatic brain injury makes the brain vulnerable to secondary insults. Post-traumatic alterations in intracranial dynamics, such as reduced intracranial compliance (IC), are thought to further potentiate the effects of secondary insults. Reduced IC combined with intracranial volume insults leads to metabolic disturbances in a rat model. The aim of the present study was to discern whether a post-traumatic hypotensive insult in combination with reduced IC caused more pronounced secondary metabolic disturbances in the injured rat brain.


METHODS
Rats were randomly assigned to four groups (n = 8/group): 1) trauma with hypotension; 2) trauma and reduced IC with hypotension; 3) sham injury with hypotension; and 4) sham injury and reduced IC with hypotension. A weight drop model of cortical contusion trauma was used. IC was reduced by gluing rubber film layers on the inside of bilateral bone flaps before replacement. Microdialysis probes were placed in the perimeter of the trauma zone. Hypotension was induced 2 h after trauma. Extracellular (EC) levels of lactate, pyruvate, hypoxanthine, and glycerol were analyzed.


RESULTS
The trauma resulted in a significant increase in EC dialysate levels of lactate, lactate/pyruvate ratio, hypoxanthine, and glycerol. A slight secondary increase in lactate was noted for all groups but group 2 during hypotension, otherwise no late effects were seen. There were no effects of reduced IC.


CONCLUSIONS
In conclusion, reduced IC did not increase the metabolic disturbances caused by the post-traumatic hypotensive insult. The results suggest that a mild to moderate hypotensive insult after initial post-traumatic resuscitation may be tolerated better than an early insult before resuscitation.
Department of Neurosurgery, Uppsala University Hospital, Uppsala, Sweden.
Konstantin
K
Salci
Per
P
Enblad
Michel
M
Goiny
Charles F
CF
Contant
Ian
I
Piper
Pelle
P
Nilsson
D000818:Animals; D001921:Brain / Q000473:pathology; D001929:Brain Edema; D001930:Brain Injuries / Q000150:complications* / Q000503:physiopathology; D004195:Disease Models, Animal; D005990:Glycerol / Q000737:chemistry; D007022:Hypotension / Q000503:physiopathology*; D019271:Hypoxanthine / Q000737:chemistry; D019344:Lactic Acid / Q000737:chemistry; D008297:Male; D019289:Pyruvic Acid / Q000737:chemistry; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
D019271:Hypoxanthine; D019344:Lactic Acid; D019289:Pyruvic Acid; D005990:Glycerol