Abstract
Cardiac anaphylaxis has been described as the increase in rate and strength of contraction and the onset of arrhythmias in isolated heart preparations from sensitised animals challenged in vitro with specific antigen. These changes in myocardial functions were explained by the release of histamine as the sole mediator,1 or by the combination of histamine release with the production of vasoactive products from the arachidonic acid cascade.2 Cardiac anaphylaxis is widely recognised as an example of type I hypersensitivity in which the release of histamine participates in myocardial damage.2 Endogenous autacoids modulate cardiac anaphylaxis. In the isolated guinea pig heart, catecholamine levels and the availability of catecholamine receptors regulate the release of histamine from sensitised hearts: depletion of catecholamines and the blockade of β-receptors decrease anaphylactic histamine release, which is enhanced by noradrenaline.1 Histamine down-regulates the anaphylactic release of histamine from sensitised guinea pig hearts: H2-receptor agonists decrease the amount of histamine released, whereas cimetidine increases it.3 It has been reported that nitric oxide (NO) modulates cardiac anaphylaxis.4 The NO donor, sodium nitroprusside, decreases anaphylactic histamine release from sensitised guinea pig hearts, which is increased by blocking nitric oxide synthase.4 Relaxin (RLX) is a peptide hormone secreted mainly by the corpus luteum during pregnancy,5 with well established effects on the female reproductive organs. Cardiomyocytes from rat atria have been shown to secrete detectable amounts of RLX suggesting the cardiovascular system as a physiological target.6
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References
Giotti A., Guidotti A., Mannaioni P.F., and Zilletti L.: The influence of andrenotropic drugs and noradrenaline on the histamine release in cardiac anaphylaxis in vitro. J Physiol Lond 184:924-941, 1966.
Capurro N. and Levi R.: The heart as a target organ in systemic allergic reactions: comparison of cardiac anaphylaxis in vivo and in vitro. Circ Res 36:520-528, 1975.
Blandina P., Brunelleschi S., Fantozzi R., Giannella E., Mannaioni P.F., and Masini E.: The antiana-phylactic action of histamine H2-receptor agonists in the guinea-pig isolated heart. Br J Pharmacol 90:459-466, 1987.
Masini E., Pistelli A., Gambassi F., Di Bello M.G., and Mannaioni P.F.: The role of nitric oxide in anaphylactic reaction of isolated guinea pig hearts and mast cells. In: Moncada S., Nisticò G., and Higgs E.A., editors, Nitric Oxide: Brain and Immune System. London and Chapel Hill, Portland Press Ltd., 277-287, 1994.
Bryant-Greenwood G.D.: Relaxin as a new hormone. Endocr Rev 3:62-90, 1992.
Taylor M.J. and Clark C.L.: Evidence for a novel source of relaxin: atrial cardiocytes. J Endocrinol 143:R5-R8, 1994.
Bigazzi M., Bani D., Bani G., and Bani-Sacchi T.: Relaxin and the cardio-circulatory system. In: MacLennan A.H., Tregear R.G., and Bryant-Greenwood, Eds. Progress in Relaxin Research. Singapore, World Scientific Publishing Co., 449-507, 1995.
Massicott G., Parent A., and St Louis J.: Blunted response to vasoconstrictors in mesenteric vasculature but not in portal vein of spontaneously hypersensitive rats treated with relaxin. Proc Soc Exp Biol Med, 190:254-259, 1988.
Bani Sacchi T., Bigazzi M., Bani D., Mannaioni P.F., and Masini E.: Relaxin-induced increased coronary flow through stimulation of nitric oxide production. Br J Pharmacol, 116:1589-1594,1995.
Masini E., Pistelli A., Gambassi F., Di Bello M.G., and Mannaioni P.F.: The role of nitric oxide in anaphylactic reaction of isolated guinea pig hearts and mast cells. Nitric Oxide: Brain and Immune System. London and Chapel Hill, Moncada S., Nisticò G., and Higgs E.A., Eds., Portland Press Ltd, 277-287, 1994.
Masini E., Bani D., Bigazzi M., Mannaioni P.F., and Bani Sacchi T.: Effects of relaxin on mast cells. In vitro and in vivo studies in rats and guinea pigs. J Clin Invest, 94:1974-1980, 1994.
Ndisang J.F., Gai P., Berni L., Mirabella C., Baronti R., Mannaioni P.F., and Masini E.: Modulation of the immunological response of guinea pig mast cells by carbon monoxide. Immunophar-macology, 43:65-73, 1999.
Stocker R., Yamamoto Y., McDonagh A.F., Glazer A.N., and Ames B.N.: Bilirubin is an antioxidant of possible physiological importance. Science 235:1043-1046, 1987.
Deinum G., Stone J.R., Babcock G.T., and Marietta M.A.: Binding of nitric oxide and carbon monoxide to soluble guanylate cyclase as observed with Resonance Raman spectroscopy. Biochemistry 35:1540-1547, 1996.
Otterbein L.O., Mantell L.L., and Choi A.M.K.: Carbon monoxide provides protection against hyperoxic lung injury. Lung Cellular and Mole-cular Physiol 276:4 L688-L694, 1999.
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© 2002 Springer Science+Business Media New York
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Vannacci, A. et al. (2002). Generation of Nitric Oxide and Carbon Monoxide Provide Protection Against Cardiac Anaphylaxis. In: Abraham, N.G. (eds) Heme Oxygenase in Biology and Medicine. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0741-3_38
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DOI: https://doi.org/10.1007/978-1-4615-0741-3_38
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