title: Role of autacoids in cardiovascular colapse in anaphylactic shock in anaesthetized dogs.
abstract: OBJECTIVE
  In anaphylactic shock (AS), the relative effects of the autacoids including histamine, prostaglandins (prost), and leukotrienes (leuk) on causing cardiovascular collapse and the extent to which receptor blocking agents and pathway inhibitors may prevent this collapse are not clear.
  
  
  METHODS
  In randomized design, we investigated whether blockade of histamine H1, H2, and H3 receptors or inhibition of the cyclooxygenase (cyclo) and lipoxygenase pathways (lipox) prevented AS in ragweed sensitized dogs. Seven dogs were studied under pentobarbital anesthesia in which the treatment studies were approximately 2 weeks apart.
  
  
  RESULTS
  During H1 receptor blockade, the decreases in blood pressure and cardiac output otherwise observed in AS were attenuated (P < 0.05) and the release of prost, thromboxanes, and leuk were reduced as compared with nontreatment studies. Cyclo inhibition also attenuated cardiovascular collapse and mediator release in AS, but the other treatments showed no effects.
  
  
  CONCLUSIONS
  H1 receptor blockade and cyclo may attenuate cardiovascular shock in AS. These agents inhibit autacoid release from mast cells in addition to any specific receptor blocking and pathway inhibition effects.
authors.affiliation: Section of Critical Care, University of Manitoba, Winnipeg, Canada. minksn@cc.umanitoba.ca
authors.forename: S
authors.initials: S
authors.lastname: Mink
authors.forename: A
authors.initials: A
authors.lastname: Becker
authors.forename: S
authors.initials: S
authors.lastname: Sharma
authors.forename: H
authors.initials: H
authors.lastname: Unruh
authors.forename: K
authors.initials: K
authors.lastname: Duke
authors.forename: W
authors.initials: W
authors.lastname: Kepron
mesh_terms: D000704:Analysis of Variance; D000707:Anaphylaxis / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D000818:Animals; D002319:Cardiovascular System / Q000503:physiopathology*; D016861:Cyclooxygenase Inhibitors / Q000627:therapeutic use*; D004285:Dogs; D006439:Hemodynamics / Q000187:drug effects; D006633:Histamine Antagonists / Q000627:therapeutic use*; D006634:Histamine H1 Antagonists / Q000627:therapeutic use; D006635:Histamine H2 Antagonists / Q000627:therapeutic use; D007211:Indoles / Q000627:therapeutic use; D007213:Indomethacin / Q000627:therapeutic use; D018836:Inflammation Mediators / Q000097:blood; D016859:Lipoxygenase Inhibitors / Q000627:therapeutic use*; D010880:Piperidines / Q000627:therapeutic use; D011804:Quinolines / Q000627:therapeutic use; D011897:Random Allocation; D011899:Ranitidine / Q000627:therapeutic use; D018100:Receptors, Histamine H3 / Q000187:drug effects
chemical_list: D016861:Cyclooxygenase Inhibitors; D006633:Histamine Antagonists; D006634:Histamine H1 Antagonists; D006635:Histamine H2 Antagonists; D007211:Indoles; D018836:Inflammation Mediators; D016859:Lipoxygenase Inhibitors; D010880:Piperidines; D011804:Quinolines; D018100:Receptors, Histamine H3; C078266:MK 0591; D011899:Ranitidine; C052075:thioperamide; D007213:Indomethacin