The Protective Effect of H2-Receptor Activation Against the Duration of Myocardial Hypoxia/Reoxygenation-Induced Ventricular Fibrillation in Sensitized Guinea-Pig Hearts

Abstract

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 H 2 -receptor antagonist inhibited the reduction of VF duration. Treatment of the non-sensitized hearts with the histamine H 2 -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 H 2 -receptor activation due to the released histamine may be involved in the protective effect.

Histamine deficiency exacerbates myocardial injury in acute myocardial infarction through impaired macrophage infiltration and increased cardiomyocyte apoptosis

“…However, a role for histamine in the pathogenesis of specific cardiovascular diseases remains controversial. Several studies suggested that histamine could be a negative factor in atherosclerosis (AS) and vascular remodeling, but few studies have directly explored the role of histamine in AMI 10 13 23 24 25 .…”