Changes of Blood Glutamate Levels in Hypoxic Ischemic Encephalopathy Patients Undergoing Brain Hypothermia

Recently, brain hypothermia therapy (BHT) has been performed for hypoxic ischemic encephalopathy (HIE) of severely asphyxiated infants, but the effect of BHT for HIE has not been established. Brain hypothermia is thought to affect the release of glutamate in the brain tissue. Therefore, we studied the changes of glutamate release in HIE infants with BHT. Brain hypothermia was performed in seven infants. In all patients a catheter was inserted into the internal jugular vein on the head side in order to monitor intracerebral temperature and take blood samples. Four infants with severe cardiopulmonary insufficiency were referred for extracorporeal membrane oxygenation (ECMO), and participated in whole-body cooling by circulating cooled blood using a heat exchanger in the ECMO circuit. Three infants underwent selective head cooling by wrapping a thermo-exchanger blanket around the head. Brain hypothermia was performed for 72 h to keep the intracerebral temperature around 35°C. Blood samples from the radial artery and cephalic vein were obtained before and during BHT. In each case blood glutamate levels were measured and the differences of those between the cephalic vein and radial artery (A blood glutamate level) evaluated, to obtain an indication of glutamate release in the brain tissue. Before BHT the blood glutamate level in the radial artery was 446.753 ± 467.178 nmol/ml and that in the cephalic vein 1094.521 ± 1114.748 nmol/ml. During BHT the blood glutamate levels in the radial artery and cephalic vein dropped to 192.129 ± 185.032 and 387.736 ± 425.490 nmol/ml, repectively. The A blood glutamate level before BHT was 647.769 ± 719.637 nmol/ml whereas that after BHT was 195.607 ± 289.357 nmol/ml, significantly low compared with before BHT (P = 0.0465). It is suggested that BHT seems to inhibit the release of blood glutamate from brain tissue in HIE cases undergoing BHT.