Leukotriene C4 Is Released from the Anaphylactic Heart: A Case for Its Direct Negative Inotropic Effect

  • Roberto Levi
  • Yuichi Hattori
  • James A. Burke
  • Zhao-Gui Guo
  • Ughetta Hachfeld del Balzo
  • William A. Scott
  • Carol A. Rouzer
Part of the GWUMC Department of Biochemistry Annual Spring Symposia book series (GWUN)


Data from our laboratory indicate that the heart reacts as a target organ in systemic hypersensitivity reactions (Capurro and Levi, 1975; Graver et al., 1983). Cardiac dysfunction observed during anaphylaxis in the guinea pig (Capurro and Levi, 1975; Zavecz and Levi, 1977) resembles that reported in humans (Bernreiter, 1959; Both and Patterson, 1970; Criep and Woehler, 1971; Petsas and Kotier, 1973; Sullivan, 1982) and is caused by mediators released intracardially and reaching the heart from the lung (Zavecz and Levi, 1977). “Cardiac anaphylaxis” (Feigen and Prager, 1969) is characterized by tachycardia, arrhythmias, contractile failure, coronary constriction, and mediator release (Capurro and Levi, 1975; Levi and Allan, 1980; Levi et al., 1982). Tachycardia and arrhythmias are caused by the release of endogenous cardiac histamine, since they are reproduced by the intracardiac administration of histamine and abolished by antihistamines (Levi and Allan, 1980; Levi et al., 1982). On the other hand, anaphylactic coronary constriction is markedly reduced by cyclooxygenase inhibitors such as indomethacin or aspirin or by thromboxane syn-thetase inhibitors such as 1-(2-isopropylphenyl)imidazole (Allan and Levi, 1981). Furthermore, the intracardiac administration of U 46619, a stable thromboxane analogue, causes coronary constriction (Allan and Levi, 1980a). Thus, prostanoate compounds, particularly thromboxane, contribute to the fall in coronary flow rate that characterizes cardiac anaphylaxis (Levi et al., 1982). Other potent coronary-constricting agents, such as platelet-activating factor (PAF, AGEPC), are also likely to contribute to anaphylactic coronary constriction (Levi et al., 1984).


Papillary Muscle Coronary Flow Negative Inotropic Effect Glyceryl Ether Coronary Flow Rate 
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Copyright information

© Springer Science+Business Media New York 1985

Authors and Affiliations

  • Roberto Levi
    • 1
  • Yuichi Hattori
    • 1
  • James A. Burke
    • 1
  • Zhao-Gui Guo
    • 1
  • Ughetta Hachfeld del Balzo
    • 1
  • William A. Scott
    • 1
  • Carol A. Rouzer
    • 1
  1. 1.Department of PharmacologyCornell University Medical College and the Rockefeller UniversityNew YorkUSA

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