title: L-arginine impacts pulmonary vascular structure in rats with an aortocaval shunt.
abstract: BACKGROUND
  The present study was designed to explore the therapeutic effect of L-arginine on the proliferation and apoptosis of pulmonary artery smooth muscle cells (SMCs) in high pulmonary blood flow-induced pulmonary hypertension and therefore to provide a basis for the mechanism by which L-arginine regulated pulmonary hypertension.
  
  
  METHODS
  Twenty-one male SD rats were randomly divided into shunting group, shunting with L-arginine group, and control group. Abdominal aorta and inferior vena cava shunting was produced in rats of the shunting group and the shunting with L-arginine group. Pulmonary artery mean pressure (mPAP) and pulmonary vascular microstructure were analyzed. Immunohistochemistry for proliferative cell nuclear antigen (PCNA) and Fas expressions and TdT-mediated dUTP-biotin nick-end labeling (TUNEL) were used to detect cell proliferation and apoptosis, respectively.
  
  
  RESULTS
  mPAP, RV/BW, and RV/LV + S were significantly increased in shunted rats compared to normal controls (P < 0.01, respectively). Pulmonary vascular structural remodeling developed in shunted rats. Proliferative index (PI), apoptotic index (AI), and the ratio of PI/AI of pulmonary artery SMCs in the rats of shunting group were elevated obviously (P < 0.01). Meanwhile, the expressing integral score of Fas was elevated in the shunting group (P < 0.01). However, L-arginine significantly attenuated pulmonary artery pressure and ameliorated pulmonary vascular structural remodeling. Also, it reduced PI and again augmented AI of pulmonary artery SMCs. The ratio of PI/AI was significantly reduced (P < 0.01). The expressing integral score of Fas was again augmented by L-arginine (P < 0.01).
  
  
  CONCLUSIONS
  L-Arginine could inhibit proliferation and promote apoptosis of pulmonary artery SMCs in shunted rats.
authors.affiliation: Department of Pediatrics, First Hospital of Peking University, Beijing, People's Republic of China.
authors.forename: Wei
authors.initials: W
authors.lastname: Bing
authors.forename: Du
authors.initials: D
authors.lastname: Junbao
authors.forename: Qi
authors.initials: Q
authors.lastname: Jianguang
authors.forename: Li
authors.initials: L
authors.lastname: Jian
authors.forename: Tang
authors.initials: T
authors.lastname: Chaoshu
mesh_terms: D000818:Animals; D001011:Aorta / Q000601:surgery; D017209:Apoptosis / Q000187:drug effects; D001120:Arginine / Q000494:pharmacology*; D001166:Arteriovenous Shunt, Surgical; D002455:Cell Division / Q000187:drug effects; D004195:Disease Models, Animal; D006976:Hypertension, Pulmonary / Q000188:drug therapy* / Q000473:pathology; D017380:Hypertrophy, Right Ventricular / Q000473:pathology; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D011651:Pulmonary Artery / Q000473:pathology*; D011652:Pulmonary Circulation; D011669:Pulmonary Wedge Pressure; D051381:Rats; D017207:Rats, Sprague-Dawley; D014682:Vena Cava, Inferior / Q000601:surgery
chemical_list: D001120:Arginine