@entity4854 , cerebrospinal fluid lactic acidosis, and cerebral blood flow in severely head-injured XXXX .

@entity1 @entity2806 @entity542 @entity880 @entity4854 @entity413
Cerebrospinal fluid (CSF) @entity880 concentration is known to increase during the acute phase after severe @entity542 . To determine the influence of glycemia or @entity2806 on this @entity880 increase, we studied 69 head-injured @entity1 aged 28.7 +/- 15.4 (SD) years with a mean Glasgow coma score of 5.7 +/- 1.7 (SD). They were intubated, paralyzed, and artificially respired. We measured @entity880 and @entity413 concentrations in ventricular CSF (VCSF), arterial blood, and jugular bulb blood for 5 days. Samples were obtained within 12 hours after injury and at regular 12-hour intervals. These @entity1 were not treated for hypo- or @entity4854 . Cerebral blood flow (CBF) was also measured within 12 hours and at 12- to 48-hour intervals. @entity4854 was found consistently within 12 hours after injury (224 +/- 98 mg/dl, P less than 0.001), and mild @entity4854 persisted during the entire period of study. The VCSF @entity413 course was parallel to that in blood (the initial VCSF @entity413 value was 128 +/- 37 mg/dl, P less than 0.001). The blood @entity880 value was also elevated during the first 12 hours (4.2 +/- 2.0 mmol/litre, P less than 0.001), normalizing within 24 to 36 hours. The VCSF @entity880 course was independent from that of the blood @entity880 value. It was significantly elevated within 12 hours after injury (5.3 +/- 2.6 mmol/litre, P less than 0.001) and remained so during the 5 days of study. A high initial VCSF @entity413 value was associated with a high initial VCSF @entity880 value. However, a high VCSF @entity880 concentration was present even when the @entity413 value was close to the normal level.(ABSTRACT TRUNCATED AT 250 WORDS)
