title: Characteristics of the in vitro hypoxic pulmonary vasoconstrictor response in isolated equine and bovine pulmonary arterial rings.
abstract: OBJECTIVE
  Hypoxaemia accompanies dorsal recumbency in the horse and frequently complicates general anaesthesia. The physiology associated with this phenomenon is poorly understood. One possible cause of poor tolerance to dorsal recumbency is an absent or reduced response to hypoxic pulmonary vasoconstriction (HPV). This study compared the HPV response in isolated pulmonary artery vessels from equivalent regions of equine and bovine lung.
  
  
  METHODS
  Equine and bovine, in vitro study.
  
  
  METHODS
  Equine and bovine pulmonary arteries were removed from the lungs of euthanased horses and cattle. Measurements of isometric tension were made on isolated rings of pulmonary vessels at 37 degrees C in a Krebs' saline solution. Hypoxia was induced by bubbling with a nominally 0% O(2) gas mixture.
  
  
  RESULTS
  A significant HPV response was observed above a baseline tension induced by phenylephrine (PE; 0.3 microm) or 5-hydroxytryptamine (5-HT; 0.1 microm). The HPV response in equine pulmonary vessels was approximately 33% less than the response observed in equivalent bovine vessels (equine 196 +/- 20%versus bovine 290 +/- 32%; p < 0.05). Removal of the endothelium (by rubbing the luminal surface) significantly reduced but did not abolish the HPV response. Incubation with the nitric oxide (NO) synthase inhibitor N-nitro-l-arginine methyl ester (L-NAME; 100 microm), or COX-1/COX-2 inhibitor indomethacin (10 microm) markedly attenuated the HPV response in equine vessels.
  
  
  CONCLUSIONS
  These results suggest that a significant HPV response exists in isolated equine pulmonary vessels; a component of this response requires a functional endothelium. Inhibition of cyclooxygenase and NO synthase attenuated the response, suggesting the involvement of a COX product and/or NO in mediating this effect either directly or indirectly. Alternatively, a non-COX related action of the nonsteroidal anti-inflammatory drug, indomethacin, may be involved.
authors.affiliation: University of Glasgow Veterinary School, Bearsden, Glasgow, Scotland G61 1QH, UK. K.MacEachern@vet.gla.ac.uk
authors.forename: Karen E
authors.initials: KE
authors.lastname: MacEachern
authors.forename: Godfrey L
authors.initials: GL
authors.lastname: Smith
authors.forename: Andrea M
authors.initials: AM
authors.lastname: Nolan
mesh_terms: D000818:Animals; D001920:Bradykinin / Q000494:pharmacology; D002417:Cattle; D002418:Cattle Diseases / Q000503:physiopathology*; D006734:Horse Diseases / Q000503:physiopathology*; D006736:Horses; D000860:Hypoxia / Q000503:physiopathology / Q000662:veterinary*; D010100:Oxygen / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011187:Posture; D011651:Pulmonary Artery / Q000187:drug effects / Q000503:physiopathology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D014662:Vasoconstrictor Agents; D010656:Phenylephrine; D010100:Oxygen; D001920:Bradykinin