ARTERIAL-JUGULAR VEIN FREE AMINO-ACID LEVELS IN PATIENTS WITH HEAD-INJURIES - IMPORTANT ROLE OF GLUTAMINE IN CEREBRAL NITROGEN-METABOLISM

Citation
Sr. Petersen et al., ARTERIAL-JUGULAR VEIN FREE AMINO-ACID LEVELS IN PATIENTS WITH HEAD-INJURIES - IMPORTANT ROLE OF GLUTAMINE IN CEREBRAL NITROGEN-METABOLISM, The journal of trauma, injury, infection, and critical care, 41(4), 1996, pp. 687-695
Citations number
16
Categorie Soggetti
Emergency Medicine & Critical Care
Volume
41
Issue
4
Year of publication
1996
Pages
687 - 695
Database
ISI
SICI code
Abstract
Traumatic brain injury is the single largest contributor of trauma cen ter deaths, Injury to the brain cannot be considered as an isolated ev ent, affecting only this organ, Profound hypoglutaminemia, commonly se en in patients with head injuries may be caused by the diminished rele ase of glutamine from the brain to the systemic circulation, To assess this hypothesis, we have simultaneously measured the free amino acid (AA) levels in systemic arterial(A, radial artery), cerebral venous (J V, jugular bulb), and systemic venous (PA, pulmonary artery) plasma in 11 adult patients with severe head injuries once within 48 hours of t he initial injury before starting nutritional support and again after 3 to 4 days of enteral feeding, Cerebral organ (A-JV) changes of AA le vels were compared with whole body systemic (A-PA) changes, Arterial t otal AA levels when compared with reported normal values are diminishe d by 46% in patients with isolated severe injuries, Cerebral outflow o f glutamine is 6% of the total AA output compared with 73% in normals, The systemic outflow of glutamine in patients with brain injuries is 28% of total AA flow, Despite this high systemic output, significant h ypoglutaminemia persists, Feeding for 3 days did not appreciable chang e the arterial plasma AA levels except that of glutamate and citrullin e. A significant (p = 0.01) linear relationship between glutamine (pro duct) and glutamate (precursor) was seen in JV samples but not in A or PA samples, The ratio of plasma glutamine to glutamate was decreased significantly only in JV during nutritional support, and this was caus ed mainly by an increase in glutamate levels, This may be owing to def ective amidation to glutamine, inasmuch as gamma aminobutyric acid (GA BA) levels were only minimally affected, Nutritional support improves the net release of glutamine from the brain, This suggests that supple menting the diet with glutamine may be beneficial to support systemic requirements in patients with severe head injuries.