Interstitial glycerol as a marker for membrane phospholipid degradation in the acutely injured human brain
a Department of Neurosurgery, b Department of Clinical Chemistry, c Department of Anesthesiology, Uppsala University Hospital,
Uppsala, Sweden
Correspondence to: Dr Lars Hillered, Department of Neurosurgery, Uppsala University Hospital, S-751 85 Uppsala, Sweden. Fax 0046 18 55 86 17; email: Lars.Hillered{at}neurokir.uu.se
Received 16 April
1997 and in revised form 2 September 1997;
Accepted 18
September 1997
OBJECTIVE
Brain interstitial glycerol was studied
as a potential marker for membrane phospholipid degradation in acute
human brain injury.
METHODS
Glycerol was measured in microdialysis
samples from the frontal lobe cortex in four patients in the
neurointensive care unit, during the acute phase after severe
aneurysmal subarachnoid haemorrhage. Microdialysis probes were inserted
in conjunction with a ventriculostomy used for routine intracranial
pressure monitoring. Clinical events involving hypoxia/ischaemia were
diagnosed by neurological signs, neuroimaging (CT and PET), and
neurochemical changes of the dialysate
for example, lactate/pyruvate
ratios and hypoxanthine concentrations.
RESULTS
Altogether 1554 chemical analyses on 518 microdialysis samples were performed. Clinical events involving
secondary hypoxia/ischaemia were generally associated with
pronounced increases (up to 15-fold) of the dialysate
glycerol concentration. In a patient with a stable condition and no
signs of secondary hypoxia/ischaemia the glycerol concentration
remained low. Simultaneous determination of glycerol in arterial plasma
samples showed that the changes in brain interstitial glycerol could
not be attributed to systemic changes and an injured blood brain barrier.
CONCLUSIONS
This study suggests that membrane
phospholipid degradation occurs in human cerebral ischaemia.
Interstitial glycerol harvested by microdialysis seems to be a
promising tool for monitoring of membrane lipolysis in acute brain
injury. The marker may be useful for studies on cell membrane injury
mechanisms mediated by for example, Ca2+ disturbances,
excitatory amino acids, and reactive oxygen species; and in the
evaluation of new neuroprotective therapeutic strategies.
© 1998 by Journal of Neurology, Neurosurgery, and Psychiatry
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