title: Hemodynamic mechanisms in anaphylaxis.
abstract: Intravenous administration of ascaris suum antigen (1 mg) as well as histamine (5 mg) was associated with rapid and marked reductions in cardiac output (QT) and systemic arterial pressure (Pa) in anesthetized mechanically ventilated dogs. When venous return was maintained constant by an external pump reservoir system, both antigen and histamine caused rapid reductions in the reservoir blood volume consistent with peripheral pooling. In addition, interruption of the splanchnic arterial inflow by occlusion of the descending thoracic aorta restored the cardiac output to control during histamine shock, whereas QT during antigen shock was unaffected by aortic occlusion, even though the circulatory failure was of similar magnitude. Therefore, we conclude that differences in responses of antigen and histamine shock to aortic occlusion indicate that mechanisms leading to peripheral pooling of blood are different with the two agents. In addition, stability of left atrial pressure following the administration of either agent, when the venous return is maintained constant, suggests that intrinsic myocardial dysfunction is not a major initiating mechanism in the two shock states studied.
mesh_terms: D000707:Anaphylaxis / Q000503:physiopathology*; D000818:Animals; D000941:Antigens / Q000494:pharmacology; D001011:Aorta / Q000502:physiology; D001200:Ascaris / Q000276:immunology; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D004285:Dogs; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D006632:Histamine / Q000494:pharmacology
chemical_list: D000941:Antigens; D006632:Histamine