Cortical brain microdialysis and temperature monitoring during hypothermic circulatory arrest in humans.
OBJECTIVE
Critical vascular surgery of the brain or the heart occasionally requires total cessation of the circulatory system. Profound hypothermia is used to protect the brain from ischaemic injury. This study explores the use of microdialysis to measure metabolic indices of ischaemia: glutamate, lactate, and pH, and cerebral temperature during profound hypothermia and circulatory arrest.


METHODS
Effluent from a microdialysis catheter placed in the cerebral cortex of three patients undergoing complete circulatory arrest was continuously sampled. Samples were pooled over 10 minute periods and glutamate and lactate concentrations were measured postoperatively. Brain temperature and pH were measured on line intraoperatively. Electroencephalography and monitoring of somatosensory evoked potentials and brainstem auditory evoked potentials were simultaneously carried out.


RESULTS
Patient 1 had normal glutamate and lactate. PH was 6.75 to 6.85 and increased to 6.9 after warming ensued. Patient 2 had raised glutamate and lactate during most measurements. The glutamate concentrations peaked at 305 microM/l at the start of the measurements and fell below 20 microM/l after warming. The lactate concentrations peaked at 680 microM/l before cooling, rose to 1040 microM/l during the cooling process, decreased to 212 microM/l during circulatory arrest, and rose again to 620 microM/l after warming. The pH started at 7.06 and continued a downward course until stabilising at a pH of 6.5 after circulatory arrest. Patient 3 had a transient, mild increase in glutamate and lactate during the cooling and warming period. pH was stable throughout.


CONCLUSIONS
Microdialysis combined with temperature and pH measurements of the cerebral cortex promises to be an important tool in detecting cerebral ischaemia. Further studies are needed to validate our findings and test the feasibility of modifying ischaemic changes.
Mendelowitsch
A
A
Neurological Institute, The George Washington University Medical Center, Washington, DC 20037, USA.
Mergner
G W
GW
Shuaib
A
A
Sekhar
L N
LN
D000136:Acid-Base Equilibrium / Q000502:physiology*; D000328:Adult; D000368:Aged; D001833:Body Temperature Regulation / Q000502:physiology*; D002545:Brain Ischemia / Q000175:diagnosis / Q000503:physiopathology; D001933:Brain Stem / Q000098:blood supply / Q000503:physiopathology; D002540:Cerebral Cortex / Q000098:blood supply / Q000503:physiopathology*; D004569:Electroencephalography; D004734:Energy Metabolism / Q000502:physiology*; D016057:Evoked Potentials, Auditory, Brain Stem / Q000502:physiology; D005073:Evoked Potentials, Somatosensory / Q000502:physiology; D005260:Female; D018698:Glutamic Acid / Q000378:metabolism; D006324:Heart Arrest, Induced; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007036:Hypothermia, Induced; D002532:Intracranial Aneurysm / Q000601:surgery; D002542:Intracranial Embolism and Thrombosis / Q000601:surgery; D007431:Intraoperative Complications / Q000175:diagnosis / Q000503:physiopathology; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D017551:Microdialysis; D008875:Middle Aged; D008991:Monitoring, Physiologic
D019344:Lactic Acid; D018698:Glutamic Acid