Post-operative monitoring of cortical taurine in patients with subarachnoid hemorrhage: a microdialysis study.
Intracerebral MD enables the retrieval of endogenous substances from the extracellular fluid (ECF) of the brain and has been demonstrated to be a sensitive technique for early detection of subtle vasospasm-induced neurometabolic abnormalities in patients with subarachnoid hemorrhage (SAH). The aim of this study was to monitor cortical extracellular concentrations of energy metabolism markers, such as glucose and lactate, neurotransmitter amino acids, such as glutamate, aspartate, GABA and taurine to identify any neurochemical patterns of cerebral ischemia. A prospective clinical study was conducted on a group of 16 patients with non-severe SAH operated on within 72 hours after initial bleeding. Following aneurysm clipping, an MD catheter was inserted in the cortical region where vasospasm could be expected to develop, and perfused with artificial CSF at 0.3 microl/min flow rate. Dialysate was collected every 6 hours and then analyzed on High Performance Liquid Cromatography (HPLC) for glucose, lactate, pyruvate, glutamate, aspartate, GABA and taurine. Mean ECF taurine concentrations ranged from 1.4 + 0.7 to 12.3 + 7.8 micromol/l in single patients: global mean value was 5.8 + 3.8 micromol/l. In this series, the highest absolute taurine value was 25.7 micromol/l, observed in a patient who developed clinical and radiological signs of cerebral ischemia. Nine patients presented clinical disturbances related to cerebral vasospasm. In this setting, representing a mild-to-moderate hypoxic condition, MD data demonstrated that lactate is the most sensitive marker of cellular energy imbalance. Increased lactate levels positively correlated with glutamate (P<0.0001), aspartate (P<0.0001), GABA (P<0.0001) and taurine (P<0.0001) concentrations. These results suggest that also in humans increased taurine levels reflect a condition of cellular stress. This study confirms that MD is a sensitive technique to reveal subtle metabolic abnormalities possibly resulting in cell damage.
De Micheli
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E
Dipartimento di Neurochirurgia, Università ed Ospedale di Verona, Italia.
Pinna
G
G
Alfieri
A
A
Caramia
G
G
Bianchi
L
L
Colivicchi
M A
MA
Della Corte
L
L
Bricolo
A
A
D000328:Adult; D002540:Cerebral Cortex / Q000378:metabolism*; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D019344:Lactic Acid / Q000378:metabolism; D017551:Microdialysis / Q000379:methods; D008991:Monitoring, Physiologic / Q000379:methods; D011184:Postoperative Period; D011446:Prospective Studies; D019289:Pyruvic Acid / Q000378:metabolism; D013345:Subarachnoid Hemorrhage / Q000378:metabolism* / Q000601:surgery; D013654:Taurine / Q000378:metabolism*
D013654:Taurine; D019344:Lactic Acid; D018698:Glutamic Acid; D019289:Pyruvic Acid