title: [Image analysis of airway remodeling and responsiveness in asthmatic guinea pig].
abstract: OBJECTIVE
  To observe the mechanism of airway remodeling and changes of airway responsiveness in guinea pig model of asthma.
  
  
  METHODS
  40 guinea pigs were randomly divided into two groups: control (20) and asthmatic group (20). After incubating with different stimulus, bilateral lung tissue section were stained with HE. Using image analysis system to measure the airway internal perimeter, wall area, external perimeter, etc. and calculate percentage of muscle shortening (PMS) according to formula.
  
  
  RESULTS
  (1) The airway wall thickness (WA/Pi) in asthmatic group and control group were (10.0 +/- 2.0) and (7.9 +/- 2.1) micrometer(2)/micrometer, respectively. The bronchial smooth muscle thickness in asthmatic group and control group were (4.8 +/- 1.5) and (3.1 +/- 2.0) micrometer(2)/micrometer, respectively. Both were statistically significant (P < 0.01). The number of bronchial smooth muscle nucleus in asthmatic group (0.012 3 +/- 0.002 7/micrometer) was higher compared with control (0.010 +/- 0.003/micrometer) (P < 0.05). (2) Responsiveness of airway smooth muscle to adenosine (represented by PMS) in asthmatic group and control were 0.34 +/- 0.07 and 0.29 +/- 0.08, respectively (P < 0.05). When combined with aminophyline, PMS in asthmatic group was 0.26 +/- 0.07. There was statistically significant difference when compared with adenosine alone (0.34 +/- 0.07) (P < 0.01). (3) PMS to acetylcholine in asthmatic group and control were 0.24 +/- 0.04 and 0.19 +/- 0.06, respectively (P < 0.05). When combined with heparin, PMS in asthmatic group was 0.20 +/- 0.04. There was statistically significant difference when compared with acetylcholine alone (0.24 +/- 0.04) (P < 0.05).
  
  
  CONCLUSIONS
  The main reason of airway remodeling in asthma is due to bronchial smooth muscle hyperplasia. Aminophylline and heparin may inhibit the responsiveness of airway to adenosine and acetylcholine respectively.
authors.affiliation: Respiratory Department, The Third School of Clinical Medicine, Beijing University, Beijing 100083, China.
authors.forename: X
authors.initials: X
authors.lastname: Zhang
authors.forename: W
authors.initials: W
authors.lastname: Yao
authors.forename: Q
authors.initials: Q
authors.lastname: He
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000241:Adenosine / Q000494:pharmacology; D000628:Aminophylline / Q000494:pharmacology; D000818:Animals; D001249:Asthma / Q000503:physiopathology*; D006168:Guinea Pigs; D006493:Heparin / Q000494:pharmacology; D066298:In Vitro Techniques; D008168:Lung / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects / Q000503:physiopathology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014665:Vasodilator Agents; D000628:Aminophylline; D006493:Heparin; D000241:Adenosine; D000109:Acetylcholine