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.
Highlights
Much research has been carried out into intermittent hypoxia and has shown that it may be imposed by physio-logical challenges, including strenuous exercise or spending time at high altitude, or by various diseases, including obstructive lung disease, asthma and systemic hypertension, myocardial infarction, stroke and cognitive dysfunction [1,2,3,4]
Our results suggested that the activation of COX with the subsequent generation of PGE2 may be involved in the pathological process during hypoxia in isolated rat atria
To determine the cardiac β1 adrenoceptor involved in the biological effect of anti β1 adrenergic antibody from patients with periodontitis upon rat atria contractility in normoxia, hypoxia and reperfusion conditions, was studied
Summary
Much research has been carried out into intermittent hypoxia and has shown that it may be imposed by physio-logical challenges, including strenuous exercise or spending time at high altitude, or by various diseases, including obstructive lung disease, asthma and systemic hypertension, myocardial infarction, stroke and cognitive dysfunction [1,2,3,4]. Intermittent hypoxia produces a myriad of favorable effects in the cardiovascular system, brain and other organ systems. These effects can be grouped into five major categories: 1) adaptation of organs and tissues responsible for oxygen uptake and transport [6], 2) proliferation and increased density of vascular networks [7], and 3) increased mitochondrial density in the brain, liver and heart [8]. 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. 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. Further studies will be needed to establish the real role of PGE2 during hypoxia injury of the heart in the course of autoimmune diseases
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