Low intracranial compliance increases the impact of intracranial volume insults to the traumatized brain: a microdialysis study in a traumatic brain injury rodent model.
OBJECTIVE
The vulnerability of the brain is considered to be increased after trauma. The present study was undertaken to determine whether intracranial volume insults in the posttraumatic period led to increased metabolic disturbances if intracranial compliance was decreased.


METHODS
A weight drop technique with a brain compression of 1.5 mm was used for injury. Intracranial compensatory volume was decreased 60 microl by placing rubber film between the dura mater and the bone. Intracranial volume insults were induced using the Bolus injection technique. Microdialysis was used to measure interstitial lactate, pyruvate, hypoxanthine, and glycerol. Fifty-two rats were allocated to trauma and sham groups with 0 to 3 layers of rubber film with and without intracranial volume insults.


RESULTS
In the groups with reduced intracranial volume exposed to intracranial volume insults, the time course of metabolic markers showed higher increases and slower recovery rates than for the other groups. Reduced intracranial volume or intracranial volume insults alone did not cause any changes compared with controls.


CONCLUSIONS
These results support the hypothesis that decreased intracranial compliance increases the vulnerability of the brain for secondary volume insults even with intracranial pressure at low levels between the insults. This finding has important clinical implications in that it stresses the need to identify patients with low intracranial compliance so that their treatment can be optimized.
Salci
Konstantin
K
Department of Neurosurgery, Uppsala University Hospital, Uppsala, Sweden.
Nilsson
Pelle
P
Goiny
Michel
M
Contant
Charles
C
Piper
Ian
I
Enblad
Per
P
D000818:Animals; D015415:Biomarkers / Q000032:analysis / Q000378:metabolism; D001921:Brain / Q000378:metabolism / Q000503:physiopathology*; D001923:Brain Chemistry / Q000502:physiology; D001929:Brain Edema / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D001930:Brain Injuries / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology*; D002462:Cell Membrane / Q000737:chemistry / Q000378:metabolism; D020202:Cerebral Hemorrhage, Traumatic / Q000378:metabolism / Q000503:physiopathology; D003187:Compliance; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000502:physiology; D045604:Extracellular Fluid / Q000378:metabolism; D005990:Glycerol / Q000032:analysis / Q000378:metabolism; D019271:Hypoxanthine / Q000032:analysis / Q000378:metabolism; D019586:Intracranial Hypertension / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology*; D019344:Lactic Acid / Q000032:analysis / Q000378:metabolism; D008297:Male; D017551:Microdialysis; D009410:Nerve Degeneration / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012886:Skull / Q000503:physiopathology*
D015415:Biomarkers; D019271:Hypoxanthine; D019344:Lactic Acid; D005990:Glycerol