The role of air pollution upon myocardial remodeling

Abstract

Technological improvement has brought an increased amount and range of agents disposed in the atmosphere. Moreover, there is a direct relationship with increased air pollution with the occurrence of deaths from heart failure, acute myocardial infarction and arrhythmias. Many studies have reported that the increase of particulate matter (PM <10nM) induces oxidative stress which can cause inflammation increasing the expression of inflammatory cytokines. Specifically, in the myocardium affected by an ischemic process, cardiomyocytes necrosis, apoptosis, activation of the complement system, inflammatory cell accumulation in the infarcted area and in remote area occurs. The pathways for this cell loss also include inflammation and oxidative stress. This complex chain of events promotes intense molecular and cellular remodeling in the infarcted region and in regions distant to it. However, the available literature does not correlate the influence of exposure to pollution with remodeling, inflammation and oxidative stress specifically in the myocardium. The aim of this study is to evaluate the role of pollution in structural, geometric and functional remodeling in the heart using an experimental model of myocardial infarction. The study will analyze the accumulation of interstitial and perivascular collagen in the myocardium, as well as inflammation, oxidative stress and apoptosis. It also will correlate these parameters with each other . 90 rats will be divided into six groups (control group, control group exposed to pollution, SHAM, infracted previously exposed to pollution and kept on that after infarction, and infarcted group immediately exposed to pollution). The methods that will be used: histology for morphometric analysis, real time RT-PCR for inflammatory cytokines and apoptosis, echocardiography for cardiac anatomy and function and ELISA to assess oxidative stress.Using the model of acute myocardial infarction in rats and exposing it to pollution during four weeks, we will have the opportunity to observe the adverse effects that such exposure can cause, more specifically upon myocardial structure and function.Using morphometry and echocardiography we will analyze how the pollution may affected the structural remodeling of myocardium and how much it may impair the myocardial function. Finally, studying the indicators of oxidative stress and inflammation we will be able to evaluate how the activation of this complex mechanism due to pollution may be responsible for changing the structure and functioning features of the heart. (AU)