PM sensitizes carotid body function in CREBA133 mice.
(A) Diaphragmatic EMG responses to brief (20 s)
exposure to 100% O2 (arrows) in
CREBA133 and CD1 mice exposed to vehicle (PBS) or PM. AP
= action potential of the diaphragmatic EMG; AU = arbitrary units; ∫EMG
= integrated diaphragmatic EMG activity. (B) Effects of
brief hyperoxia (Dejour's test) on minute neural respiration (MNR). Data
are mean ± SEM change in MNR (MNR100% –MNR21%
O2)/MNR21%O2. n = 4 mice per
group (*P < 0.05). (C and
D) Integrated sensory activities of the carotid
body in response to hypoxia in CD1 and CREBA133 mice exposed
to PBS or PM (Po2 = partial pressures of
O2 in the perfusate [Po2 = 50 mm
Hg]). Black bars represent duration of the hypoxic
challenge. The superimposed action potential of a “single” fiber is
shown (inset). Average sensory responses to graded
hypoxia are presented as changes in impulses/second (hypoxia –
baseline). Values are mean ± SEM. *P < 0.05. n =
Number of fibers analyzed from five mice per group. (E)
PM induces dysregulation of inflammatory, oxidant, and carotid body
regulatory genes in CD1 and CREBA133 mice. Pooled carotid
body RNA from PBS- and PM-challenged CD1 and CREBA133 mice
(36 h; n = 10–12 mice per group) was used in qPCR
reactions (see Materials and
Methods). Shown are expression levels for IL-6, Toll-like
Receptor 2 (TLR2), heme oxygenase (Hmox1), superoxide dismutase (SOD2),
the large conductance Ca2+–activated K+ channel
(Kcnd2), and the Na+–Ca2+ exchanger 1 precursor
protein (Slc8a1). Data represent the fold change in gene expression
compared with PBS-challenged CD1 mice (*P <
0.05).