Effect Of Arginine Vasopressin On Cerebral Edema Following Traumatic Brain Injury

Brain edema is the complex reaction following traumatic brain injury, including vasogenic edema,cytotoxic edema, Osmatic edema and interstitial edema. It has a crucial impact on morbidity and mortality as it increases intracranial pressure, impairs cerebral perfusion and oxygenation, and contributes to additional ischemic injuries. Moreover the mechanism and treatment of traumatic brain edema still remains pulsed.Arginine vasopressin has been known to be a neuropeptide which regulate fluid and ionic environment and volume, cardiovascular function, balance of temperature, behavior of study and mermroy, secretion of ACTH. The actions of vasopressin are mediated by stimulation of tissue-specific G protein-coupled receptors. V₁R receptor is the main receptor in the central nervous system. It has been recently suggested that AVP and its receptors have a vital role on traumatic brain injury and traumatic brain edema Thus the study is resigned to observe the serial concentration of AVP in plasma following acute traumatic brain injury in combination with the clinical symptom, the imaging data and the Glasgow Outcome Scale(GOS) in order to investigate the role of AVP on brain edema after traumatic brain injury and seek the efficient treatment of it.Subject and Method1. Patients: A total of 45 cases with acute traumatic brain injury hospitalized in Sir Run Run Shaw Hospital were enrolled in our study from Jan 2004 to Aug 2005. There were 20 female and 25 males, aged from 20 to 65 years old with a mean age of 42.5. The including criteria.? Hospitalized within 12 ours after brain injury;?Confirmed by CT scanning, MRI or operation;?Without severe combination of other organ injuries;?Without complication of severe dysfunction of heart, lung, kidney and other important organs;?Without severe diseases history before injury. All the cases were found as cerebral contusions and lacerations including 12 cases with simply cerebral contusions, 6 cases combined with epidural hematomas, 7 cases combined with subdural hematomas. and 20 cases combined with encephalic hematomas. The severity of head injury was scored by Glasgow Coma Score (GCS). There are 19 patents with GCS >8 (the moderately injured group) and 26 with GCS^ 8 (the severely injured group). 30 healthy volunteers who had negative founding at medical examination in our hospital at the same period were enrolled as the control group. There were 18 males and 12 females, aged from 25 to 66 years with a mean age of 40 years.2. Sample collection and measurement: Blood samples were obtained by venipuncture at 12h, 3d, 5d after cerebral injury. The samples were collected in pre-cooled centrifuge tubescontaining 50ul of 0.3mol/l ethylene diamine teracetic acid sodium (EDTA-Na) and 5X105 traylol, centrifuged at 3000r/min for 10 min at 4°C and stored at -70°C. After all the samples needed had been collected, measurements were taken by radioimmunoassay. The plasma level of AVP was measured at Hangzhou Radioimmunologic Center. The radioimmunoassay reagent bits were purchased by DSL company in USA and the y -radioimmunologic counting meter is by American DPC company. The measurement procedures were taken according to the instructions of the bits. All the samples were marked and measured by the double blind method.3. Imaging data analysis: Brain CT scan were made to all the patients as soon as they were sent to emergency department and were rechecked every 2 or 3 days at the time of hospitalizatioa The peak time of the cerebral edema was estimated by the record and measurement of the cerebral edema area at the CT scan. The severity of the cerebral edema was classified according to the ratio of the maximal cerebral edema length (from the lesion edge to the edema edge) to the maximal cerebral lesion length* including: Grade 1, 00.05).ConclusionThe plasma AVP level increases in the traumatic brain injury patients. AVP may play a role on brain edema after traumatic brain injury: the higher AVP increases, the more severity the brain edema persist, and the worse the outcome is. It is impossible to efficiently control the traumatic brain edema by use of AVP antagonist.