Author(s)

Sabrina Ganzinelli, Silvia Reina, Mirian Matoso, Germán González, Celina Morales, Enri Borda

Institute of Cardiovascular Physiopathology, School of Medicine, University of Buenos Aires, Buenos Aires, Argentina.
National Research Council of Argentina (CON-ICET), Buenos Aires, Argentina; Institute of Cardiovascular Physiopathology, School of Med-icine, University of Buenos Aires, Buenos Aires, Argentina.
Pharmacology Unit, School of Dentistry, Uni-versity of Buenos Aires, Buenos Aires, Argentina; National Research Council of Argentina (CON-ICET), Buenos Aires, Argentina.

Background: Hypoxia is one of the most frequently encountered stresses in health and disease. Methods: We compared the effects of an anti-β₁ periodontal IgG (pIgG) and an authentic β₁ adrenergic agonist, xamoterol, on isolated myocardium from rat atria contractility. We used an ELISA assay to measure the generation of PGE₂ 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: PGE₂ generation increased during the hypoxia and was unchanged during reoxygenation period compared with the production of this prostanoid in atria during normoxia condition. A β₁ specific adrenoceptor antagonist atenolol and the β₁ 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 PGE₂ was dependent on the activation of cox-1 and cox-2 isoforms. Moreover, cox-2 was more active and produced more increments in the production of PGE₂ 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 performed and showed tissue necrosis and edematization at the myocardium level. Conclusion: The phenomenon studied here supports the notion that PGE₂ may be responsible for tissue edematization. PGE₂ maybe acts as a beneficial modulator in the myocardium and prevents a major injury of it. The inflammation damage to the heart organ and cardiomyocytes caused by the actions of the antibodies in the course of heart lesions provoked by cardiovascular autoimmune disease, explains some of these results obtained in the present experiments. Further studies will be needed to establish the real role of PGE₂ during hypoxia injury of the heart in the course of autoimmune diseases.

Myocardium; PGE₂; Hypoxia; Histopathology; Periodontitis; Antibodies Anti-β₁ Adrenoceptors; Xamoterol

S. Ganzinelli, S. Reina, M. Matoso, G. González, C. Morales and E. Borda, "PGE₂ Generation in Myocardium from Isolated Rat Atrium under Hypoxia and Reoxygenation Conditions. Effect of Anti-β₁ IgG from Patients with Chronic Severe Periodontitis," Pharmacology & Pharmacy, Vol. 5 No. 2, 2014, pp. 204-215. doi: 10.4236/pp.2014.52027.