title: Comparison of dopamine and norepinephrine after traumatic brain injury and hypoxic-hypotensive insult.
abstract: After severe brain trauma, blood-brain barrier disruption and alteration of cerebral arteriolar vasoreactive properties may modify the cerebral response to catecholamines. Therefore, the goal of the present study was to compare the effects of dopamine and norepinephrine in a model of brain injury that consisted of a weight-drop model of injury complicated by a 15-min hypoxic-hypotensive insult (HH). Sprague-Dawley rats (n = 7 in each group) received, after brain injury, an infusion of either norepinephrine (TNE group) or dopamine (TDA group) in order to increase cerebral perfusion pressure (CPP) above 70 mm Hg. In addition, a control group (C group, no trauma) and a trauma group (T group, brain injury, no catecholamine infusion) were studied. Mean arterial pressure (MAP), intracranial pressure (ICP, intraparenchymal fiberoptic device), and local cerebral blood flow (LCBF, extradural laser-Doppler fiber) were measured throughout the protocol. In T group, brain injury and HH induced a decrease in CPP (by an increase of ICP and a decrease of MAP), and a decrease of LCBF. Both norepinephrine and dopamine failed to increase CPP, and ICP was significantly higher in TNE and TDA groups than in T group. Interestingly, norepinephrine was not able to alleviate the decrease in MAP. Neither norepinephrine or dopamine could induce an increase of MAP. LCBF decreased similarly in T, TNE and TDA groups. In conclusion, norepinephrine and dopamine are not able to restore values of CPP above 70 mm Hg in a model of severe brain trauma. Furthermore, their systemic vasopressor properties are altered.
authors.affiliation: Réanimation Médicale, Hôpital Broussais, Paris, France.
authors.forename: C
authors.initials: C
authors.lastname: Ract
authors.forename: B
authors.initials: B
authors.lastname: Vigué
authors.forename: N
authors.initials: N
authors.lastname: Bodjarian
authors.forename: J X
authors.initials: JX
authors.lastname: Mazoit
authors.forename: K
authors.initials: K
authors.lastname: Samii
authors.forename: M
authors.initials: M
authors.lastname: Tadié
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001921:Brain / Q000473:pathology / Q000503:physiopathology; D001930:Brain Injuries / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology; D004298:Dopamine / Q000627:therapeutic use*; D002534:Hypoxia, Brain / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D019585:Intracranial Hypotension / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D007427:Intracranial Pressure / Q000187:drug effects; D009638:Norepinephrine / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012121:Respiration, Artificial; D014662:Vasoconstrictor Agents / Q000627:therapeutic use*
chemical_list: D014662:Vasoconstrictor Agents; D004298:Dopamine; D009638:Norepinephrine