COMPARISON OF BRAIN-TISSUE OXYGEN-TENSION TO MICRODIALYSIS-BASED MEASURES OF CEREBRAL-ISCHEMIA IN FATALLY HEAD-INJURED HUMANS

Citation
Ab. Valadka et al., COMPARISON OF BRAIN-TISSUE OXYGEN-TENSION TO MICRODIALYSIS-BASED MEASURES OF CEREBRAL-ISCHEMIA IN FATALLY HEAD-INJURED HUMANS, Journal of neurotrauma, 15(7), 1998, pp. 509-519
Citations number
41
Categorie Soggetti
Neurosciences,"Clinical Neurology","Emergency Medicine & Critical Care
Journal title
ISSN journal
08977151
Volume
15
Issue
7
Year of publication
1998
Pages
509 - 519
Database
ISI
SICI code
0897-7151(1998)15:7<509:COBOTM>2.0.ZU;2-S
Abstract
This study investigated the relationship between brain tissue oxygen t ension (PbtO(2)) and cerebral microdialysate concentrations of several compounds in five patients with refractory intracranial hypertension after severe head injury. The following substances were assayed: lacta te and glucose; the excitatory amino acids glutamate and aspartate; an d the cations potassium, calcium, and magnesium. Glucose concentration s did not correlate with PbtO(2), but lactate increased as PbtO(2) dec reased. The lactate/glucose ratio exhibited a close relationship to Pb tO(2), increasing sharply only when oxygen tension reached zero. Altho ugh glucose and oxygen eventually reached very low levels and zero, re spectively, in these fatally head-injured patients, the terminal decre ase in PbtO(2) slightly preceded that of glucose in four of the five p atients. This time lag is the cause of the poor correlation between gl ucose and PbtO(2). Glutamate and aspartate concentrations both demonst rated a close relationship to PbtO(2), with sharp increases not occurr ing until PbtO(2) was zero. Concentrations of these amino acids exhibi ted a similar pattern in response to decreasing glucose concentrations . Potassium concentrations began increasing at a PbtO(2) of 35 mm Hg, which is not generally considered indicative of hypoxia. Sharper incre ases began occurring once PbtO(2) dropped below 15 mm Hg, with a sligh t rise in the minimum potassium concentrations recorded at these low P btO(2) values. Calcium and magnesium concentrations did not vary in re sponse to PbtO(2). In summary, the most robust biochemical indicators of cerebral anoxia were elevations in the lactate/glucose ratio and in the concentrations of lactate and of the excitatory amino acids gluta mate and aspartate. Furthermore, the fact that glucose concentrations continue to decrease for a short period after oxygen levels reach zero suggests that cells continue to utilize glucose anaerobically for suc h functions as maintenance of cellular integrity, with collapse of the cell membrane as evidenced by increases of extracellular glutamate an d aspartate not occurring until both oxygen and glucose concentrations reach zero.