Bell M J, Robertson C S, Kochanek P M, Goodman J C, Gopinath S P, Carcillo J A, Clark R S, Marion D W, Mi Z, Jackson E K
Safar Center for Resuscitation Research and the University of Pittsburgh Brain Trauma Research Center, University of Pittsburgh, Pittsburgh, PA, USA.
Crit Care Med. 2001 Feb;29(2):399-404. doi: 10.1097/00003246-200102000-00033.
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.
Study of critically ill adults with severe traumatic brain injury.
Adult neurointensive care unit.
We prospectively defined periods of normal saturation and desaturation in six patients after severe traumatic brain injury.
During these periods, cerebral microdialysis samples of brain interstitial fluid were collected, and adenosine and purine metabolites were measured by high-pressure liquid chromatography.
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 (r(2) =.32,.14,.31,.07, and.26, respectively, all p <.05, Pearson product moment correlation).
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.
腺苷可降低脑氧代谢率并增加脑血流量，其可能在创伤性脑损伤后对低灌注的脑代谢和脑血管反应中发挥重要作用。创伤性脑损伤后监测颈静脉血氧饱和度以评估脑氧摄取情况，血氧饱和度降低可能反映继发性脑损伤。我们推测在颈静脉血氧饱和度降低（<50%）期间，脑间质腺苷及相关嘌呤代谢产物会增加，并确定嘌呤、乳酸和葡萄糖之间的关联，以评估腺苷在人类继发性损伤中的作用。
对患有严重创伤性脑损伤的危重症成人进行研究。
成人神经重症监护病房。
我们前瞻性地定义了6例严重创伤性脑损伤患者的血氧饱和度正常和降低的时期。
在这些时期内，采集脑间质液的脑微透析样本，并用高压液相色谱法测量腺苷和嘌呤代谢产物。
在血氧饱和度降低期间，腺苷增加了3.1倍，黄嘌呤增加了2.5倍（与正常血氧饱和度时期相比，两者p均<.05，符号秩检验）。在两个研究时期，腺苷、黄嘌呤、次黄嘌呤和环磷酸腺苷均与乳酸相关（r²分别为.32、.14、.31、.07和.26，均p<.05，Pearson积矩相关）。
颈静脉血氧饱和度降低期间脑间质腺苷显著增加，提示腺苷可能在创伤性脑损伤后的继发性损伤期发挥重要作用。这些代谢产物与乳酸的相关性进一步表明，在糖酵解代谢增强期间腺苷会增加。
