Chinese Journal of Emergency Medicine 2009;18(12):1266-1269
doi:10.3760/cma.j.issn.1671-0282.2009.12.009
Changes of VE-cadherin and arginine vasopressin in patients with acute brain injuries
Li LI ; Youmin HUANG
Keywords
VE-cadherin; Arginine vasopressin; Brain injuries; Brain edema; Prognosis
Country
China
Language
Chinese
Abstract
Objective To observe the changes of serum vascular endothelium-cadherin (VE-cadherin) and plasma arginine vasopressin (AVP) in patients with acute brain injury, and to investigate the VE-cadherin and plasma AVP related to brain edema and prognosis following acute brain injury. Method ELISA was used to measure the serum VE-cadherin level and radioimmunoassay was used to measure serial concentration of AVP in plasma of 110 patients with acute brain injury 12 hours and 3 and 5 days after brain injury. The outcome was estimated in combination of clinical manifestation, iconographic findings and Glasgow Outcome Scale (GOS). Results The levels of VE-cadherin and AVP increased significantly over 12 hours after brain injury with reduction of GCS. The severer brain injury resulted in higher levels of VE-cadherin and AVP, and prolongation of peak brain edema (P < 0.01). VE-cadherin levels showed positive correlation with severity of brain edema (r = 0.69, P < 0.01) and prolongation of brain edema (r = 0.70.P < 0.01). AVP levels had positive correlation with severity of brain edema (r = 0.65, P < 0.01) and prolongation of brain edema (r = 0.64, P < 0.01). Furthermore, there were significant increases in VE-cadherin and AVP levels in patients with low GOS groups (P < 0.01). The VE-cadherin and AVP leveb in poor outcome group persistently increased for 5 days after brain injury and were higher than those in good outcome group and normal control group. There were a correlation between VE-cadherin and AVP in patients with acute brain injury (r = 0.75, P < 0.01). Conclusions VE-cadherin and AVP leveb are closely associated with the prognosis of patients after acute brain injury. VE-cadherin and AVP may play pivotal roles in the pathogenesis of brain edema after acute brain injury.
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