A continuous exposure to urban air pollution aggravates myocardial infarction in mice: the role of lung inflammation and impaired cardiac mitochondrial function

MARCHINI, TIMOTEO; GARCÉS, MARIANA; MAGNANI, NATALIA; KELLY, JAZMIN; PAZ, MARIELA; LAGO, NESTOR; MARGIOTTIELLO, DANIEL; CACERES, LOURDES; CALABRO, VALERIA; VICO, TAMARA; VANASCO, VIRGINIA; ALVAREZ, SILVIA; GONZALEZ MAGLIO, DANIEL; BERRA, ALEJANDRO; GELPI, RICARDO; EVELSON, PABLO

Ciudad de Buenos Aires

Congreso; LXIII Reunión Científica Anual; 2018

Sociedad Argentina de Investigación Clínica

Air pollution exposure is associated with increased mortality due to myocardial infarction (MI). It has been suggested that breathing polluted air leads to pulmonary and systemic inflammation, which might affect MI progression. To address this hypothesis, we evaluated the contribution of a continuous exposure to air pollution over experimental MI in mice, with particular focus over lung inflammation and cardiac mitochondrial function. Male eight-week-old BALB/c mice were exposed to filtered air (FA, control) or urban air (UA) inside whole-body inhalation chambers located in a highly populated area of Buenos Aires City for up to 16 weeks. After 8 weeks, mice breathing UA showed a 56% increase in total leucocyte count in bronchoalveolar lavage (BAL) samples (FA: 1.0±0.2 x105 cells, p