Weigand M A, Michel A, Eckstein H H, Martin E, Bardenheuer H J
Department of Anesthesiology, University of Heidelberg, Germany.
Anesthesiology. 1999 Aug;91(2):414-21. doi: 10.1097/00000542-199908000-00015.
For the human brain, there are no data available concerning the significance of adenosine and its metabolites as biochemical indicators of cerebral ischemia. Since adenosine may counteract key pathogenetic mechanisms during cerebral ischemia, its sensitivity and specificity as a marker of cerebral ischemia was investigated in relation to hypoxanthine and lactate.
Arterial and jugular venous concentration changes of adenosine, hypoxanthine, and lactate were studied in 41 patients undergoing carotid endarterectomy. Cerebral tissue oxygenation was monitored continuously by somatosensory-evoked potentials. A carotid artery shunt (n = 6) was placed only after complete loss of somatosensory-evoked potentials.
Before carotid artery clamping jugular venous concentrations of adenosine, hypoxanthine, and lactate in subsequently shunted patients were 229+/-88 nM, 1105+/-116 nM, and 0.85+/-0.52 mM, respectively (mean +/- SD). In patients who required shunting, carotid artery clamping induced a significant increase in jugular venous adenosine (389+/-114 nM) and jugular venous hypoxanthine (1444+/-168 nM). In contrast, the increase in jugular venous lactate (0.91+/-0.48 mM) did not reach statistical significance. Focal cerebral ischemia was indicated by jugular venous adenosine with a sensitivity and specificity of 0.83 and 0.71, respectively.
Carotid artery clamping induced significant increases in jugular venous adenosine and hypoxanthine in patients with inadequate collateral blood flow. In addition, focal cerebral ischemia was reflected by changes in adenosine concentrations.
