PGE2 Generation in Myocardium from Isolated Rat Atrium under Hypoxia and Reoxygenation Conditions. Effect of Anti-β1 IgG from Patients with Chronic Severe Periodontitis

SABRINA GANZINELLI; SILVIA REINA; MIRIAN MATOSO; GERMÁN E. GONZÁLEZ; CELINA MORALES; ENRI BORDA

Pharmacology & Pharmacy

Scientific Research Publishing

Año: 2014 p. 204 - 215

2157-9423

Background: Hypoxia is one of the most frequently encountered stresses in health and disease. Methods: We com-pared the effects of an anti-β1 periodontal IgG (pIgG) and an authentic β1 adrenergic agonist, xamoterol, on iso-lated 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 histopathological-ly in the presence of both the antibody and/or the adrenergic agonist drug during normoxia, hypoxia and reperfu-sion 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 adreno-ceptor 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 activa-tion 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 or- gan and cardiomyocytes caused by the actions of the antibodies in the course of heart lesions provoked by cardiovas- cular 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