Abstract
The secondary injury cascades exacerbating the initial brain injury following intracerebral haemorrhage (ICH) are incompletely understood. We used dual microdialysis (MD) catheters placed in the perihaemorrhagic zone (PHZ) and in seemingly normal cortex (SNX) at time of surgical ICH evacuation in ten patients (range 26–70 years). Routine interstitial MD markers (including glucose and the lactate/pyruvate ratio) were analysed and remaining microdialysate was analysed by two-dimensional gel electrophoresis (2-DE) and nano-liquid chromatography tandem mass spectrometry (nLC-MS/MS). Two time intervals were analysed; median 2–10 hours post-surgery (time A) and median 68–76 hours post-ICH onset (time B). Using 2-DE, we quantified 232 ± 31 different protein spots. Two proteins differed between the MD catheters at time A, and 12 proteins at time B (p < 0.05). Thirteen proteins were significantly altered between time A and time B in the SNX and seven proteins in the PHZ, respectively. Using nLC-MS/MS ca 800 proteins were identified out of which 76 were present in all samples. At time A one protein was upregulated and two downregulated, and at time B, seven proteins were upregulated, and four downregulated in the PHZ compared to the SNX. Microdialysis-based proteomics is feasible for study of secondary injury mechanisms and discovery of biomarkers after ICH.
Highlights
The secondary injury cascades exacerbating the initial brain injury following intracerebral haemorrhage (ICH) are incompletely understood
A cascade of secondary injury factors is initiated by products of the coagulation cascade and ICH breakdown products, in particular thrombin, which results in microglia activation within hours[11]
Typical pre- and post-operative computed tomography (CT) scans are shown in Fig. 1a,b, where the placement of the two MD catheters is shown
Summary
The secondary injury cascades exacerbating the initial brain injury following intracerebral haemorrhage (ICH) are incompletely understood. We used dual microdialysis (MD) catheters placed in the perihaemorrhagic zone (PHZ) and in seemingly normal cortex (SNX) at time of surgical ICH evacuation in ten patients (range [26–70] years). A cascade of secondary injury factors is initiated by products of the coagulation cascade and ICH breakdown products, in particular thrombin, which results in microglia activation within hours[11]. These activated cells in turn release factors that induce breakdown of the blood-brain barrier, exacerbate the vasogenic oedema formation and induce apoptosis in both neurons and glia[11].
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