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Young hearts are as susceptible as old hearts to the direct and acute cardiotoxic effects of ultrafine air pollutants
Author(s) -
Simkhovich Boris Z,
Kleinman Michael T,
Kloner Robert A
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.lb105
Subject(s) - medicine , air pollutants , population , cardiology , air pollution , chemistry , environmental health , organic chemistry
Environmental exposure to air pollutants triggers cardiac events and increases cardiac morbidity and mortality in the general population. We hypothesized that age might become a key factor in cardiotoxic effects triggered by air pollutants. Experiments were carried out in Langendorff‐perfused hearts obtained from young (4 month old) and aged (26 months old) Fisher/Brown Norway rats. Standard diesel particulate matter (National Institute of Standards and Technology) was filtered for ultrafine particles (UP; <0.1 μ) and suspended in perfusion buffer. Four groups of hearts were studied: young and old control buffer‐perfused hearts (YC, OC), and young and old hearts perfused for 30 min with UP (YUP, OUP). Control hearts demonstrated a slight decrease in developed pressure by17% and 8% in YC and OC groups (from 122±9 to 102±13 mmHg and from 133±7 to 123±9 mmHg respectively; p<0.05 vs. baseline), while UP perfused hearts showed a dramatic fall by 33% and 35% in YUP and OUP groups (p<0.05 vs. control). Positive dP/dt remained stable in both control groups, but was decreased by 28% in YUP and OUP groups (p<0.05 vs. control). Coronary flow was significantly decreased in both UP groups (by 28% in YUP and by 26% in OUP groups; p<0.05 vs. control). These results indicate that both young and old hearts were equally susceptible to direct and acute cardiotoxic effects of ultrafine air pollutants. Supported by US EPA Grant No. RD‐83195201.