Hemodynamic mechanisms in anaphylaxis

S. Enjeti, E. R. Bleecker, P. L. Smith, J. Rabson, S. Permutt, R. J. Traystman

Research output: Contribution to journalArticle

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 (Q̇(T)) and systemic arterial pressure (P̄(a)) 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 Q̇(T) during antigen shock was unaffected by aortic occlusion, even though the circulatory failure was of similar magnitude. Therefore, we conclude that differences in response 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.

Original languageEnglish (US)
Pages (from-to)297-309
Number of pages13
JournalCirculatory Shock
Volume11
Issue number4
StatePublished - Dec 1 1983

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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    Enjeti, S., Bleecker, E. R., Smith, P. L., Rabson, J., Permutt, S., & Traystman, R. J. (1983). Hemodynamic mechanisms in anaphylaxis. Circulatory Shock, 11(4), 297-309.