title: Effect of heartworm infection on in vitro contractile responses of canine pulmonary artery and vein.
abstract: OBJECTIVE
  To test the effect of heartworm infection on agonist-induced constriction of canine pulmonary artery and vein in vitro.
  
  
  METHODS
  Cumulative concentration-response relations to norepinephrine, serotonin, histamine, prostaglandin F2 alpha, and the thromboxane A2 analog U-44069 were determined, using isolated rings of pulmonary artery and vein from control and heartworm-infected dogs. To determine the role of endothelial cells in histamine constriction, some rings were denuded of endothelial cells in both artery and vein.
  
  
  METHODS
  Noninfected control and heartworm-infected dogs.
  
  
  RESULTS
  There was no difference in constriction response to norepinephrine, serotonin, prostaglandin F2 alpha, or U44069 of pulmonary artery or vein from control or heartworm-infected dogs. Histamine-induced constriction of pulmonary artery from heartworm-infected dogs was not different from control values, however, when endothelial cells were removed from control, but not heartworm-infected pulmonary artery, histamine-induced constriction was enhanced. Histamine-induced constriction of pulmonary vein from heartworm-infected dogs was significantly depressed, compared with that of control pulmonary vein. However, removal of endothelial cells in pulmonary vein from heartworm-infected, but not control dogs significantly increased constriction.
  
  
  CONCLUSIONS
  Heartworm infection alters histamine-induced constriction responses of pulmonary artery and vein. These changes may reflect high circulating histamine concentrations in heartworm-infected dogs, compared with that in controls. Increased circulating histamine concentrations in vivo could bring about decreased sensitivity of histamine receptors o decreases in the number of receptors expressed.
  
  
  CONCLUSIONS
  Mast cells and histamine may be important factors in altered endothelium-mediated responses associated with heartworm disease.
authors.affiliation: Department of Physiology, Michigan State University, East Lansing 48824-1101, USA.
authors.forename: D S
authors.initials: DS
authors.lastname: Maksimowich
authors.forename: M
authors.initials: M
authors.lastname: Mupanomunda
authors.forename: J F
authors.initials: JF
authors.lastname: Williams
authors.forename: L
authors.initials: L
authors.lastname: Kaiser
mesh_terms: D000818:Animals; D015237:Dinoprost / Q000494:pharmacology; D004183:Dirofilaria immitis / Q000302:isolation & purification; D004184:Dirofilariasis / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D004283:Dog Diseases / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D006632:Histamine / Q000494:pharmacology; D066298:In Vitro Techniques; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000469:parasitology / Q000502:physiology; D009638:Norepinephrine / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D011450:Prostaglandin Endoperoxides, Synthetic / Q000494:pharmacology; D011651:Pulmonary Artery / Q000187:drug effects / Q000469:parasitology / Q000503:physiopathology*; D011667:Pulmonary Veins / Q000187:drug effects / Q000469:parasitology / Q000503:physiopathology*; D012701:Serotonin / Q000494:pharmacology; D013928:Thromboxane A2 / Q000031:analogs & derivatives; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*
chemical_list: D011450:Prostaglandin Endoperoxides, Synthetic; D012701:Serotonin; C028429:U 44069; D013928:Thromboxane A2; D011189:Potassium Chloride; D006632:Histamine; D015237:Dinoprost; D009638:Norepinephrine