Interstitial brain adenosine and xanthine increase during jugular venous oxygen desaturations in humans after traumatic brain injury

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Abstract

Objective

Adenosine decreases the cerebral metabolic rate for oxygen and increases cerebral blood flow, and it may play an important role in cerebrometabolic and cerebrovascular responses to hypoperfusion after traumatic brain injury. Jugular venous oxygen saturation is monitored after traumatic brain injury to assess brain oxygen extraction, and desaturations may reflect secondary brain insults. We hypothesized that brain interstitial adenosine and related purine metabolites would be increased during jugular venous oxygen saturation desaturations (<50%) and determined associations between the purines, lactate, and glucose to assess the role of adenosine during secondary insults in humans.

Design

Study of critically ill adults with severe traumatic brain injury.

Setting

Adult neurointensive care unit.

Patients

We prospectively defined periods of normal saturation and desaturation in six patients after severe traumatic brain injury.

Interventions

During these periods, cerebral microdialysis samples of brain interstitial fluid were collected, and adenosine and purine metabolites were measured by high-pressure liquid chromatography.

Measurements and Main Results

Adenosine increased 3.1-fold and xanthine increased 2.5-fold during desaturation periods (both p < .05 vs. normal saturation period, signed rank). Adenosine, xanthine, hypoxanthine, and cyclic-adenosine monophosphate correlated with lactate over both study periods (r2 = .32, .14, .31, .07, and .26, respectively, all p < .05, Pearson product moment correlation).

Conclusion

The marked increases in interstitial brain adenosine that occur during jugular venous oxygen desaturations suggest that adenosine may play an important role during periods of secondary insults after traumatic brain injury. The correlation of these metabolites with lactate further suggests that adenosine is increased during periods of enhanced glycolytic metabolism.

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