1 ts) had end-tidal CO2 obtained by oral/nasal
sidestream capnometry, and respiratory rates, oxygen sat
2 ral KCs exposed for 24 h to aged and diluted
sidestream cigarette smoke (ADSS) or an equivalent conce
3 We reported that gestational exposure to
sidestream cigarette smoke (SS), or secondhand smoke, pr
4 ce were exposed for 4 weeks to either air or
sidestream cigarette smoke (SS; 5 mg/m(3) total particul
5 posed to filtered air or to aged and diluted
sidestream cigarette smoke as a surrogate to environment
6 lingual microcirculation was assessed with a
Sidestream Dark Field imaging device before and after RB
7 Sublingual
Sidestream Dark Field imaging was performed to determine
8 l microcirculation was evaluated by means of
sidestream dark field imaging.
9 blingual microcirculation was observed using
sidestream dark-field imaging, and peripheral tissue per
10 microcirculatory blood flow was assessed by
sidestream dark-field imaging.
11 We performed
sidestream dark-field videomicroscopy of the sublingual
12 lingual microcirculation was evaluated using
sidestream dark-field videomicroscopy.
13 luated (at baseline, 6, 12, and 18 hr) using
sidestream dark-field videomicroscopy.
14 Microvascular imaging using sublingual
sidestream darkfield imaging (SDF) and endothelial funct
15 ed using orthogonal polarization spectral or
sidestream darkfield imaging techniques.
16 Here, we used
Sidestream Darkfield imaging to detect changes in glycoc
17 d platelets less than high-tar extracts, the
sidestream extracts were almost equally potent.
18 lets subjected to mainstream smoke extracts,
sidestream extracts, and nicotine was measured in vitro
19 tual pilot-scale granular sludge reactor for
sidestream nitritation, but significantly underestimated
20 End-tidal PCO2 was measured, using a
sidestream sensor placed in line of the ventilator circu
21 known about the effects of acute exposure to
sidestream smoke (passive smoking).
22 Sidestream smoke exposure significantly augmented the pe
23 Mainstream and
sidestream smoke extracts caused increased platelet acti
24 ere measured before and during inhalation of
sidestream smoke in one session (n = 16) and before and
25 Rats were exposed to
sidestream smoke in smoking chambers.
26 The source of ETS was
sidestream smoke of 4 cigarettes/15 min, 6 h/day, 5 days
27 We examined the effects of
sidestream smoke on muscle sympathetic nerve activity (M
28 ed to ETS in a chamber in which steady-state
sidestream smoke was continuously circulating.
29 Sidestream smoke, but not vehicle inhalation, increased
30 he stressful stimuli were not potentiated by
sidestream smoke, except for an increased BP response to
31 After 15 minutes' exposure to
sidestream smoke, plasma nicotine and carboxyhemoglobin
32 both in smokers and in nonsmokers exposed to
sidestream smoke.
33 BP, and HR were not changed significantly by
sidestream smoke.
34 Acute short-term passive (
sidestream)
smoke exposure elicits a modest increase in
35 phen [100 mg/kg intraperitoneal (ip)] and/or
sidestream tobacco smoke (as a surrogate for ETS, 5 mg/m
36 term exposure to mainstream tobacco smoke or
sidestream tobacco smoke (STS), the main component of se
37 Guinea-pigs were chronically exposed to
sidestream tobacco smoke (surrogate for environmental to
38 onary C-fibre endings by chronic exposure to
sidestream tobacco smoke is transmitted to the NTS and i
39 n shown to be present in both mainstream and
sidestream tobacco smoke using an EM-MS system.
40 dimensional or organ culture were exposed to
sidestream whole (SSW) smoke, a major component of secon