title: [Effects of iptkalim, a novel ATP-sensitive potassium channel opener, on hypoxia-induced pulmonary vascular remodeling in rats].
abstract: OBJECTIVE
  To investigate whether pulmonary vascular remodeling in hypoxic pulmonary hypertensive rats could be prevented by treatment with a selective K(ATP)CO, iptkalim (Ipt).
  
  
  METHODS
  Rats were fed in hypoxic and normobaric environment (10% +/- 0.5% O2, 8 h/day and 6 day/week) and divided into control group, hypoxia group (hypoxic rat treated with ig NS 5.0 ml x kg(-1) x d(-1)), treated group I (hypoxic rat treated with ig Ipt 0.75 mg x kg(-1) x d(-1)), treated group II (hypoxic rat treated with ig Ipt 1.5 mg x kg(-1) x d(-1)). After 4 wk, the mean pulmonary arterial pressure (mPAP), right ventricle/left ventricle and septum [RV/(LV + S)] were measured, and the small pulmonary arterial morphologic changes were observed with morphometric analysis under microscopes in four groups.
  
  
  RESULTS
  The level of mPAP and RV/(LV+ S) was significantly higher in the hypoxic group than those in control group (P < 0.01). Morphometric analysis revealed that the ratio of vascular medial wall thickness to external diameter (MT%) and the ratio of vascular medial cross-sectional area to total arterial cross-sectional area (MA%) were also significantly increased in the hypoxic group than those in control group (P < 0.01) and the ratio of vessel lumen cross-sectional area to total arterial cross-sectional area (VA%) was significantly lower in the hypoxic group than those in control group (P < 0.01). Ipt 0.75 mg x kg(-1) x d(-1) or 1.5 mg x kg(-1) x d(-1) decreased the level of mPAP(mmHg), RV/(LV+ S), and inhibited the small pulmonary arterial remodeling significantly. Ipt 1.5 mg x kg(-1) x d(-1) reversed all pathological indices.
  
  
  CONCLUSIONS
  K(ATP)CO iptkalim can be a very promising candidate for the treatment of hypoxic pulmonary hypertension.
authors.affiliation: Department of Pulmonology, The First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China.
authors.forename: Wei-Ping
authors.initials: WP
authors.lastname: Xie
authors.forename: Hong
authors.initials: H
authors.lastname: Wang
authors.forename: Hai
authors.initials: H
authors.lastname: Wang
authors.forename: Bai-Zhou
authors.initials: BZ
authors.lastname: Li
authors.forename: Gang
authors.initials: G
authors.lastname: Hu
mesh_terms: D000818:Animals; D006976:Hypertension, Pulmonary / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology*; D000860:Hypoxia / Q000503:physiopathology*; D054086:KATP Channels / Q000819:agonists*; D008297:Male; D011437:Propylamines / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D054086:KATP Channels; C502260:N-(1-methylethyl)-1,1,2-trimethylpropylamine; D011437:Propylamines