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Cardiovascular Research 1999 43(1):173-182; doi:10.1016/S0008-6363(99)00073-5
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Role of autacoids in cardiovascular collapse in anaphylactic shock in anesthetized dogs

S. Minka,b,c,*, A. Beckere, S. Sharmaa,b, H. Unruhf, K. Dukeb,c and W. Kepronb,c,d

aSection of Critical Care, University of Manitoba, Winnipeg, MB, Canada
bSection of Respiratory Disease, University of Manitoba, Winnipeg, MB, Canada
cDepartment of Internal Medicine, University of Manitoba, Winnipeg, MB, Canada
dSection of Allergy and Immunology, University of Manitoba, Winnipeg, MB, Canada
eDepartment of Pediatrics, University of Manitoba, Winnipeg, MB, Canada
fSection of Thoracic Surgery, University of Manitoba, Winnipeg, MB, Canada

* Corresponding author. Tel.: +1-204-787-2914; fax: +1-204-787-4826 minksn{at}cc.umanitoba.ca

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. Conclusion: 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.

KEYWORDS Vasculature; Pathophysiology; Shock; Hemodynamics; Immunology; Prostaglandins; Pulmonary circulation


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