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Ultrafine particulate matter inhalation induces remote microvascular dysfunction
Author(s) -
Nurkiewicz T.R.,
Porter D.W.,
Barger M.,
Hubbs A.F.,
Millecchia L.,
Rao K.,
Chen B.T.,
Frazer D.,
Castranova V.,
Boegehold M.A.
Publication year - 2006
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.20.5.a1150-a
Subject(s) - inhalation , ultrafine particle , inhalation exposure , endothelium , particulates , medicine , in vivo , arteriole , chemistry , endocrinology , anesthesia , microcirculation , biology , organic chemistry , microbiology and biotechnology
We have shown that pulmonary exposure to fine particulate matter (PM) impairs endothelium dependent dilation in systemic arterioles. The purpose of this study was to determine if ultrafine PM inhalation produces greater microvascular dysfunction than fine PM. Our inhalation chamber creates stable TiO 2 aerosols at concentrations up to 20 mg/m 3 . TiO 2 is a well characterized particle devoid of soluble metals. Rats were exposed to fine or ultrafine TiO 2 (mean particle diameters of ~1 μm, and ~160 nm, respectively) at concentrations to produce equivalent pulmonary loads of 0.25 mg/rat. The spinotrapezius muscle was prepared for in vivo microscopy 24 hours after pulmonary exposure. Intraluminal infusion of the Ca 2+ ionophore A23187 was used to evaluate endothelium dependent arteriolar dilation (micropipette ejection pressures of 5, 10, 20 and 40 psi). In control rats, A23187 infusion produced dose dependent arteriolar dilations that were near maximal at 40 psi. In rats exposed to fine TiO 2 , A23187 infusion failed to elicit a significant arteriolar response. In rats exposed to ultrafine TiO 2 , A23187 infusion produced dose dependent arteriolar constrictions that were significantly different from the responses observed in rats exposed to fine TiO 2 . These observations suggest that at equivalent pulmonary loads, compared to fine TiO 2 , ultrafine TiO 2 inhalation produces greater remote microvascular dysfunction. This effect may be due to alterations in endothelial integrity and/or signaling. Support: Health Effects Institute #4730