PGE₂ Generation in Myocardium from Isolated Rat Atrium under Hypoxia and Reoxygenation Conditions. Effect of Anti-<i>β</i>₁ IgG from Patients with Chronic Severe Periodontitis

Abstract

Background : Hypoxia is one of the most frequently encountered stresses in health and disease. Methods : We compared the effects of an anti- β 1 periodontal IgG (pIgG) and an authentic β 1 adrenergic agonist, xamoterol, on isolated myocardium from rat atria contractility. We used an ELISA assay to measure the generation of PGE 2 in vitro after the addition of either the antibody or the adrenergic agonist. We analyzed the myocardium histopathologically in the presence of both the antibody and/or the adrenergic agonist drug during normoxia, hypoxia and reperfusion conditions. Results : PGE 2 generation increased during the hypoxia and was unchanged during reoxygenation period compared with the production of this prostanoid in atria during normoxia condition. A β 1 specific adrenoceptor antagonist atenolol and the β 1 synthetic peptide abrogated the increment of the prostanoid in the presence of pIgG but only atenolol due to it in the presence of xamoterol. The increment of PGE 2 was dependent on the activatio n of cox -1 and cox- 2 isoforms. Moreover, cox -2 was more active and produced more increment s in the productio n of PGE 2 in the presence of the pIgG than cox -1 activation. Histopathologically , studies of myocardium specimens during these different periods of the experimental protocol: basal (B), hypoxia (H) and reoxygenation (R), were also pe r formed and showed tissue necrosis and edematization at the myocardium level. Conclusion : The phenomenon studied here supports the notion that PGE 2 may be responsible for tissue edematization. PGE 2 maybe acts as a b eneficial modulator in the myocardium and prevent s a major injury of it. The inflammation damage to the heart or gan and cardiomyocytes caused by the actions of the antibodies in the course of heart lesions provoked by cardiovas cular autoimmune disease, explain s some of these results obtained in the present experiments. Further studies will be needed to establish the real role of PGE 2 during hypoxia injury of the heart in the course of autoimmune diseases .