title: Effects of anisodamine on the expressions of vascular endothelial growth factor and intercellular adhesion molecule 1 in experimental infusion phlebitis.
abstract: BACKGROUND
  Infusion phlebitis is the most common side effect of clinical intravenous drug therapy and several clinical studies have demonstrated that anisodamine can effectively prevent the occurrence of infusion phlebitis. This study was designed to investigate effects of anisodamine on the expressions of vascular endothelial growth factor (VEGF) and intercellular adhesion molecule 1 (ICAM-1) in a rabbit model of infusion phlebitis and to analyze the mechanisms of anisodamine effect on the prevention and treatment of experimental infusion phlebitis.
  
  
  METHODS
  Twenty-four specific pathogen-free male Japanese white rabbits were randomly assigned to the control group, the model group, the magnesium sulfate group and the anisodamine group. The rabbit model of infusion phlebitis, induced by intravenous administration, was established and expressions of VEGF and ICAM-1 were determined and contrasted with the control group treated with normal saline. We evaluated expression by histopathology, immunohistochemistry, reverse transcription-polymerase chain reaction, and Western blotting assay.
  
  
  RESULTS
  Pathohistological changes of the model group were observed, such as loss of venous endothelial cells, inflammatory cell infiltration, edema and thrombus. The magnesium sulfate group and the anisodamine group showed significant protective effects on vascular congestion, inflammatory cell infiltration, proliferation, swelling of endothelium and perivascular hemorrhage. The model group showed the highest expressions of VEGF and ICAM-1 of the four groups (P < 0.01). On the contrary, anisodamine alleviated the inflammatory damage by significantly reducing the expressions of VEGF and ICAM-1 compared with the model group (P < 0.01). There was no significant difference in the expressions of VEGF and ICAM-1 between the magnesium sulfate group and the anisodamine group (P > 0.05).
  
  
  CONCLUSIONS
  Anisodamine alleviates inflammatory damage by significantly reducing the expressions of VEGF and ICAM-1, and shows significant protective effects in an animal model of infusion phlebitis.
authors.affiliation: Nursing College, Zhengzhou University, Zhengzhou, Henan 450052, China. zhangzx6666@126.com
authors.forename: Zhen-Xiang
authors.initials: ZX
authors.lastname: Zhang
authors.forename: Peng
authors.initials: P
authors.lastname: Wang
authors.forename: Qiu-Shi
authors.initials: QS
authors.lastname: Zhang
authors.forename: Xue
authors.initials: X
authors.lastname: Pan
authors.forename: Qing-Xia
authors.initials: QX
authors.lastname: Zhao
authors.forename: Xiao-Kai
authors.initials: XK
authors.lastname: Wang
mesh_terms: D000818:Animals; D015153:Blotting, Western; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism*; D008297:Male; D010689:Phlebitis / Q000188:drug therapy*; D011817:Rabbits; D011897:Random Allocation; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012991:Solanaceous Alkaloids / Q000627:therapeutic use*; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*
chemical_list: D012991:Solanaceous Alkaloids; D042461:Vascular Endothelial Growth Factor A; C003922:anisodamine; D018799:Intercellular Adhesion Molecule-1