TITLE:
PGE2 Generation in Myocardium from Isolated Rat Atrium under Hypoxia and Reoxygenation Conditions. Effect of Anti-β1 IgG from Patients with Chronic Severe Periodontitis
AUTHORS:
Sabrina Ganzinelli, Silvia Reina, Mirian Matoso, Germán González, Celina Morales, Enri Borda
KEYWORDS:
Myocardium; PGE2; Hypoxia; Histopathology; Periodontitis; Antibodies Anti-β1 Adrenoceptors; Xamoterol
JOURNAL NAME:
Pharmacology & Pharmacy,
Vol.5 No.2,
February
19,
2014
ABSTRACT: 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.