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 TiO2 aerosols at concentrations up to 20 mg/m3. TiO2 is a well characterized particle devoid of soluble metals. Rats were exposed to fine or ultrafine TiO2 (mean particle diameters of approximately 1 um, and approximately 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 Ca2+ 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 TiO2, A23187 infusion failed to elicit a significant arteriolar response. In rats exposed to ultrafine TiO2, A23187 infusion produced dose dependent arteriolar constrictions that were significantly different from the responses observed in rats exposed to fine TiO2. These observations suggest that at equivalent pulmonary loads, compared to fine TiO2, ultrafine TiO2 inhalation produces greater remote microvascular dysfunction. This effect may be due to alterations in endothelial integrity and/or signaling.
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