title: The protective effect of H2-receptor activation against the duration of myocardial hypoxia/reoxygenation-induced ventricular fibrillation in sensitized guinea-pig hearts.
abstract: Patients with high serum immunoglobulin E levels were reported to be protected against sudden death during acute myocardial infarction. The protection mechanism might be attributed to the facilitation of histamine release from sensitized mast cells; however, this remains to be clarified. In this study, we examined the influence of sensitization on ventricular fibrillation (VF) induced by myocardial hypoxia/reoxygenation (H/R). Guinea pigs were actively sensitized by subcutaneous injection of ovalbumin in Bordetella pertussis vaccine. Hearts isolated from non-sensitized and sensitized guinea pigs were subjected to 30-min hypoxia / 30-min reoxygenation using a Langendorff apparatus. The amount of histamine released in the sensitized guinea-pig hearts was elevated, and the duration of VF was found to be reduced. The treatment with a histamine H2-receptor antagonist inhibited the reduction of VF duration. Treatment of the non-sensitized hearts with the histamine H2-receptor agonist resulted in the decrease of VF duration to the same level as that in the sensitized hearts. In conclusion, these results suggest that the risk of sudden death during myocardial H/R may be attenuated in the sensitized hearts and that histamine H2-receptor activation due to the released histamine may be involved in the protective effect.
authors.affiliation: Department of Pharmacology, Faculty of Pharmaceutical Sciences, Tokushima Bunri University, Japan. imajo@ph.bunri-u.ac.jp
authors.forename: Naoki
authors.initials: N
authors.lastname: Imajo
authors.forename: Saori
authors.initials: S
authors.lastname: Matsui
authors.forename: Yumiko
authors.initials: Y
authors.lastname: Yasui
authors.forename: Nobuaki
authors.initials: N
authors.lastname: Matsui
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Fukuishi
authors.forename: Masaaki
authors.initials: M
authors.lastname: Akagi
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001262:Atenolol / Q000494:pharmacology; D003594:Cytoplasmic Granules / Q000187:drug effects; D017259:Dimaprit / Q000031:analogs & derivatives / Q000494:pharmacology; D004562:Electrocardiography / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D006168:Guinea Pigs; D006632:Histamine / Q000494:pharmacology; D017442:Histamine Agonists / Q000494:pharmacology*; D006633:Histamine Antagonists / Q000494:pharmacology; D006637:Histamine N-Methyltransferase / Q000037:antagonists & inhibitors; D006636:Histamine Release / Q000187:drug effects; D007073:Immunoglobulin E / Q000378:metabolism; D066298:In Vitro Techniques; D008407:Mast Cells / Q000187:drug effects; D015428:Myocardial Reperfusion Injury / Q000150:complications*; D010477:Perfusion; D011970:Receptors, Histamine H2 / Q000187:drug effects*; D014693:Ventricular Fibrillation / Q000209:etiology* / Q000517:prevention & control*
chemical_list: D000319:Adrenergic beta-Antagonists; D004791:Enzyme Inhibitors; D017442:Histamine Agonists; D006633:Histamine Antagonists; D011970:Receptors, Histamine H2; C024535:SK&F 91488; D007073:Immunoglobulin E; D001262:Atenolol; D006632:Histamine; D006637:Histamine N-Methyltransferase; D017259:Dimaprit