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J Neurol Neurosurg Psychiatry 1998;64:611-618 doi:10.1136/jnnp.64.5.611
  • Paper

Cortical brain microdialysis and temperature monitoring during hypothermic circulatory arrest in humans

  1. A Mendelowitscha,c,
  2. G W Mergnerb,
  3. A Shuaiba,
  4. L N Sekhara
  1. aNeurological Institute, bDepartment of Anesthesiology, The George Washington University Medical Center, Washington, DC, USA, cNeurosurgical University Clinic, Basel, Switzerland
  1. Dr Gertrud W Mergner, Department of Anesthesiology, The George Washington University Medical Center, 901 23rd Street NW, Washington DC 20037, USA. Telephone 001 202 994 3134; fax 001 202 994 7003; email mergner{at}gwis.circ.gwu.edu
  • Received 6 November 1996
  • Revised 2 October 1997
  • Accepted 20 October 1997

Abstract

OBJECTIVES 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 μM/l at the start of the measurements and fell below 20 μM/l after warming. The lactate concentrations peaked at 680 μM/l before cooling, rose to 1040 μM/l during the cooling process, decreased to 212 μM/l during circulatory arrest, and rose again to 620 μM/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.

CONCLUSION 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.

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