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1.
Lung tissue resistance (Rti) measured in air-filled guinea pig lungs by the alveolar capsule technique was a large part of total lung resistance (Rl), and we wondered whether similar results applied to saline-filled lungs. We used the micropuncture method to measure alveolar
pressure (Palv) in saline-filled lungs of 21 guinea pigs. Palv and airway opening pressure (Pao) were measured before and after a sudden interruption of flow during an inflation or deflation maneuver. On stopping flow,
there was an immediate large change in Pao followed by a smaller slower change in Pao. Palv was nearly constant immediately after flow interruption but followed the slower change in Pao. The initial change in Pao on flow interruption was interpreted as the resistive pressure loss in the airways. The small change in Pao and Palv was interpreted as the pressure loss caused by tissue stress adaptation. Airway resistance (Raw) and Rti were obtained by dividing the pressure losses by the flow before the interruption. Rl was the sum of Raw and Rti. The calcium blocker nifedipine reduced both Raw and Rti and abolished the difference in Rti between inflation and deflation. Values of Rti were 10–29% of Rl. However, with correction for viscosity, Rti predicted in air-filled lungs would dominate Rl.
Accepted for publication: 21 February 1997 相似文献
2.
In newborn infants, group B streptococci (GBS) often cause pneumonia, with polymorphonuclear leukocytes (PMN) migrating into
the lungs. Because surfactant therapy may be needed in such patients, we evaluated the interaction between GBS or GBS-stimulated
PMN and a surfactant preparation (Curosurf) in vitro. The superoxide production of GBS strains or GBS-activated PMN was measured, using the nitroblue tetrazolium (NBT) test and
the subsequent lipid peroxidation (LPO) as the content of malondialdehyde (MDA) and 4-hydroxyalkenals (4-HNE). The growth
of GBS in surfactant was determined and related to the LPO. Finally, the effect of LPO on surfactant activity, caused by GBS-stimulated
PMN, was assessed by measuring dynamic surface tension in a pulsating bubble surfactometer. Curosurf diminished the NBT reduction
by both live GBS and GBS-stimulated PMN. Surfactant was peroxidized by reactive oxygen species (ROS) from both GBS and GBS-stimulated
PMN in a time-dependent manner. Vitamin E significantly reduced the peroxidation level of surfactant in both cases. Surfactant
peroxidation was associated with a reduction in the number of live bacteria. The biophysical activity of Curosurf was impaired
by GBS-stimulated PMN, as reflected by increased minimum surface tension during cyclic compression. These findings indicate
that Curosurf undergoes LPO by ROS produced by GBS and/or PMN. We speculate that exogenous surfactant preparations should
be supplemented with vitamin E or another antioxidant, when given to infants with GBS pneumonia.
Accepted for publication: 21 August 2000 相似文献
3.
Atypical Adrenoceptor-mediated Relaxation of Canine Pulmonary Artery Through a Cyclic Adenosine Monophosphate–dependent Pathway 总被引:1,自引:0,他引:1
To determine whether functional atypical β-adrenoceptors (β3-adrenoceptors) are present in pulmonary vascular smooth muscle, we studied isolated canine pulmonary arterial rings under
isometric conditions in vitro. Addition of β-adrenoceptor agonists produced a concentration-dependent relaxation of noradrenaline-precontracted
tissues, a rank order potency being isoproterenol (1) > salbutamol (0.95) > selective β3-adrenoceptor agonists, CL 316243 (0.85), and BRL 37344 (0.83). A marked desensitization to salbutamol occurred by pretreatment
with salbutamol but not with CL 316243. When β1-adrenoceptors had been blocked, the relaxant responses to salbutamol were competitively antagonized by the β2-adrenoceptor antagonist ICI 118551 with a pA2 value of 7.67 ± 0.21 (mean ± S.E.), but the response to CL 316243 was weekly antagonized by ICI 118551 only at a high concentration
of 10−5 M, where an apparent pA2 value was 5.24. In contrast, cyanopindolol, a nonselective β-adrenoceptor antagonist, antagonized CL 316243–induced relaxation
in a competitive manner with a pA2 of 6.10 ± 0.11. This pA2 value was lower than that when salbutamol was used as an agonist (6.69 ± 0.14, p < 0.01). Intracellular 3′,5′-cyclic adenosine monophosphate (cAMP) levels were increased by CL 316243 in a concentration-dependent
fashion, an effect that was not altered by ICI 118551. These results suggest that β3-adrenoceptors may exist in canine pulmonary artery smooth muscle and that stimulation of this atypical receptor causes vasodilation
through a cAMP-dependent pathway.
Accepted for publication: 17 June 1999 相似文献
4.
Pituitary adenylate cyclase–activating peptide 38 (PACAP 38) displays several biologic activities relevant to obstructive
airway disease. Carbon monoxide (CO) has recently emerged as a potent, endogenously produced mediator of bronchodilation.
In this study, we have analyzed the occurrence of PACAP 38 and the corresponding occurrence of heme oxygenase (HO), the rate-limiting
enzyme for CO production, in guinea pig trachea, using immunocytochemistry. We have also investigated whether the dilatory
effects of PACAP 38 are dependent on CO, using an in vitro setup for tracheal studies. A moderate supply of PACAP-like immunoreactive
nerve fibers was seen in association with tracheal smooth muscle. HO-like immunoreactivity was observed in the respiratory
epithelium and in association with smooth muscle bundles. PACAP 38 induced a concentration-dependent relaxation of precontracted
tracheal segments. This dilation was nearly abolished after pretreatment with zincprotoporphyrine, an inhibitor of heme oxygenase.
The same effect was accomplished with Rp-8Br-cyclicGMPS, an inhibitor of cyclicGMP, whereas the nitric oxide synthase inhibitor
NG-monomethyl-l-arginine had no effect on the PACAP 38–induced dilation. The presented data suggest that PACAP 38 can induce bronchodilation
by means of a CO-dependent, cyclicGMP-related mechanism, thereby providing a link between neurotransmission and local CO release
in the airway smooth muscle.
Accepted for publication: 10 January 2001 相似文献
5.
The purpose of this study is to determine if the polymorphonuclear leukocyte (PMN) is a major causative agent for lipopolysaccharide
(LPS)-induced lung injury and responsible for the excess production of superoxide anion in the lung. We measured superoxide
anion production from the lung and pulmonary capillary permeability in rats with and without PMN depletion. The superoxide
anion production from the lung was measured using a purpose-built ex vivo chemiluminescence apparatus. Pulmonary capillary
permeability was evaluated by the Evans blue dye extravasation method. PMN sequestration was determined by counting PMNs in
histologic tissue specimens using microscopy. All rats received 3 mg/kg LPS intravenously. Examinations were undertaken at
2, 6, and 12 h after the LPS injection. The PMN-depleted group received cyclophosphamide 4 days before the LPS injection,
which resulted in a PMN count of less than 200 cells/μl. In rats without PMN depletion, Evans blue dye extravasation increased
significantly at 12 h after the LPS injection; PMN sequestration increased at 2, 6, and 12 h after the LPS injection; and
superoxide anion production increased at 6 h and remained elevated at 12 h after the LPS injection. The increased permeability,
PMN sequestration, and superoxide anion production were not seen in the PMN-depleted group. The contribution of the xanthine/xanthine
oxidase system and alveolar macrophages to the observed superoxide anion production was negligible. We conclude that, in rats,
the PMN is a major causative agent in LPS-induced lung injury and is responsible for the excess production of superoxide anion
in the lung.
Accepted for publication: 3 March 1997 相似文献
6.
Silica inhalation predisposes workers to bacterial infection and impairments in pulmonary defense function. In this study,
we evaluated the effect of pre-exposure to silica on lung defense mechanisms by use of a rat pulmonary Listeria monocytogenes infection model. Male Fischer 344 rats were exposed by inhalation to filtered air or silica (15 mg/m3× 6 h/day × 5 days/wk). After 21 or 59 days of silica exposure, the rats were inoculated intratracheally with 5 × 103
L. monocytogenes. At 0 (noninfected controls), 3, and 7 days after infection, the left lungs were removed, homogenized, and the number of
viable L. monocytogenes was counted after an overnight culture at 37° C. Bronchoalveolar lavage (BAL) was performed on the right lungs. Alveolar
macrophages (AM) were collected, and the AM production of chemiluminescence (CL), an index of reactive oxygen species generation,
was measured. The number of lavagable neutrophils (PMNs) and acellular BAL lactate dehydrogenase (LDH) activity were determined
as indices of inflammation and injury, respectively. Pre-exposure to silica for 59 days caused substantial increases in PMN
number and LDH activity compared with the air controls, whereas silica inhalation for both 21 and 59 days significantly enhanced
the pulmonary clearance of L. monocytogenes compared with air controls. Dramatic elevations were also observed in zymosan- and phorbol myristate acetate (PMA)–stimulated
CL production by lung phagocytes recovered from rats pre-exposed to silica for 59 days. These results demonstrate that short-term
exposure to inhaled silica particles activates lung phagocytes, as evidenced by increases in reactive oxygen species. This
up-regulation in the production of antimicrobial oxidants is likely responsible for the enhancement in pulmonary clearance
of L. monocytogenes observed with short-term silica inhalation.
Accepted for publication: 2 October 2000 相似文献
7.
The dose dependence and time course of smoke inhalation injury were determined in a rabbit model. Animals were insufflated
with 18–90 breaths of cotton smoke or room air (control) at a rate of 18 breaths/min and tidal volume of 12 ml/kg. Smoke-exposed
animals exhibited dose-related histologic effects with progressive deterioration of respiratory function during the postexposure
period of observation (96 h). The smoke-exposed rabbits had reproducible injuries to both airway mucosa and lung parenchyma,
manifested by disruption and sloughing of airway and alveolar epithelia, and exudation of protein-rich fluid and leukocytes
into the airway and alveolar spaces. Significant effects were evident by 24 h postexposure. Smoke inhalation also affected
the respiratory burst of alveolar macrophages. Generation of superoxide anions by alveolar macrophages at 48 h postexposure
was increased significantly after smoke inhalation (54 breaths). The present rabbit model should be useful for studying the
interactions between pulmonary epithelial cells and leukocytes after smoke inhalation and for determining the role that abnormal
functioning of alveolar macrophages plays in the development of smoke inhalation injury.
Accepted for publication: 8 October 1998 相似文献
8.
Development of Monocrotaline-Induced Pulmonary Hypertension Is Attenuated by a Serotonin Receptor Antagonist 总被引:2,自引:0,他引:2
The significance of serotonin in the pathogenesis of monocrotaline-induced pulmonary hypertension (MCT-PH) in rats, plasma
serotonin concentrations, and the effect of a serotonin receptor antagonist administration in association with the number
of proliferative cells were investigated. The thickness of the media of the small pulmonary arteries and the weight ratio
of the RV to that of LV + S (RV/[LV + S] weight ratio) were used as indices of the severity of PH. Plasma serotonin concentrations
were measured by high-performance liquid chromatography. Histopathologic analysis of the lung tissue was performed by hematoxylin-eosin
and elastin van Gieson staining. Immunohistopathologic staining for proliferating cell nuclear antigen (PCNA) was performed
to identify proliferative cells. The severity of PH as determined by the medial thickness of the small pulmonary arteries
and RV/(LV + S) weight ratio in rats with MCT-PH was significantly reduced after treatment with MCI-9042 (p < 0.01 and p < 0.05, respectively). The serotonin concentration was significantly greater in MCT-PH rats than in normal control rats (p < 0.05). The scores for histopathologic changes, such as thickening of the alveolar walls and interstitial inflammatory cell
infiltration in MCT-PH rats, were significantly reduced after treatment with MCI-9042 (p < 0.05 and p < 0.01, respectively). The number of PCNA-positive cells was significantly greater in MCT-PH rats than in normal control
rats (p < 0.0001) and was reduced after treatment with MCI-9042 (p < 0.0001). Treatment with MCI-9042 significantly inhibited the development of MCT-PH along with a decrease in the number
of PCNA-positive cells, suggesting a pivotal role of serotonin in the development of PH induced by MCT.
Accepted for publication: 10 November 1999 相似文献
9.
The effect of administering prostaglandin E1 (PGE1) on the extent of monocrotaline (MCT)-induced pulmonary hypertension and cytokine production [interleukins (IL) 1 and 6 and
tumor necrosis factor (TNF)] by macrophages during MCT induction of pulmonary hypertension was studied. Right ventricle/left
ventricle plus septum weight ratios (RV/LV + S) were used as an index of the development of pulmonary hypertension. Administering
PGE1 at a dose of 0.2 mg/kg/day for 4 weeks reduced significantly the RV/LV + S ratio from 0.428 ± 0.070 to 0.243 ± 0.059 (p < 0.01) and decreased the production of these cytokines: IL-1, from 4.675 ± 3.558 to 1.800 ± 0.722 units; IL-6, from 0.322
± 0.121 to 0.060 ± 0.039 units; and TNF, from 0.578 ± 0.369 to 0.004 ± 0.004 units. In another series of experiments, a significant
reduction of the RV/LV + S ratio was noted for only 1 week when we administered PGE1 immediately after the injection of MCT. We confirmed that histopathologic improvements of lungs were noted by administering
0.2 mg/kg PGE1 for 4 weeks. In another experiment, PGE1 at a concentration of 2 μg/ml suppressed a rise in the cytosolic Ca2+ concentration of lipopolysaccharide-stimulated peritoneal macrophages of rats in vitro, suggesting that PGE1 suppressed cytokine production by macrophages through the suppression of the Ca2+ influx. These results suggest that administering PGE1 may be effective in the treatment of some forms of pulmonary hypertension in humans.
Accepted for publication: 20 August 1998 相似文献
10.
Elimination of Neutrophils by Apoptosis During the Resolution of Acute Pulmonary Inflammation in Rats 总被引:2,自引:0,他引:2
Y. Ishii K. Hashimoto A. Nomura T. Sakamoto Y. Uchida M. Ohtsuka S. Hasegawa M. Sagai 《Lung》1998,176(2):89-98
We evaluated the apoptosis of neutrophils during the resolution of acute pulmonary inflammation induced by exposure to ozone.
The inflammatory response was assessed in rat lungs 0, 1, 3, and 7 days after 4-h exposure to air or 2 ppm ozone. Analysis
of bronchoalveolar lavage fluid demonstrated significant increases in albumin concentrations on days 0 and 1 and in the number
of lavageable neutrophils on days 0, 1, and 3, indicating the presence of acute pulmonary inflammation. These parameters returned
to control values on day 7, which suggests that the acute pulmonary inflammation induced by ozone was reversible. On days
1 and 3, but not on day 0, the neutrophils showed morphologic evidence of apoptosis. Based on morphologic analysis, the proportion
of apoptotic neutrophils was 23.3 ± 2.2% on day 1 and 55.7 ± 3.2% on day 3. Terminal deoxynucleotidyl transferase-mediated
dUTP end labeling (TUNEL), in contrast, revealed that the proportion of apoptotic cells was 59.7 ± 9.1% on day 1 and 68.0
± 4.3% on day 3. On day 3, light microscopy and electron microscopy demonstrated engulfment of the neutrophils by macrophages.
These findings indicate that the apoptosis of neutrophils followed by their engulfment by macrophages contributes to the clearance
of neutrophils from the sites of inflammation. Moreover, TUNEL detected apoptotic neutrophils with greater sensitivity compared
with morphologic assessment.
Accepted for publication: 4 June 1997 相似文献
11.
Leukotrienes (LTs), tachykinins (TKs), and oxygen radicals have been suggested to be important modulating factors for the
hyperpnea-induced bronchoconstriction (HIB) of guinea pigs. In this study, we tested the hypothesis that LTs and oxygen radicals
modulate HIB by triggering TK release. Eighty-five Hartley guinea pigs were divided into four groups: control, dimethylthiourea
(DMTU), FPL 55712, and A63162. DMTU is the scavenger for hydroxyl radical. FPL 55712 is an antagonist of LT receptor, whereas
A63162 is an inhibitor of lipoxygenase. Each group was further divided into three subgroups: baseline, hyperpnea, and recovery.
Each animal was anesthetized, cannulated, paralyzed, and artificially ventilated. We measured dynamic respiratory compliance
(Crs), maximal expiratory flow at 50% total lung capacity (Vmax50), and forced expiratory volume in 0.1 s (FEV0.1) during the baseline and recovery periods. Hyperpnea caused significant decreases in Crs, Vmax50, and FEV0.1, indicating HIB in the control group. Pretreatment with DMTU, FPL 5712, or A63162 attenuated HIB. Plasma substance P (SP)
levels increased progressively during the experiment in all groups. However, both FPL 55712 and A63162, but not DMTU, significantly
decreased SP levels. Similarly, lung malondialdehyde (MDA) contents increased progressively during the experiment in the control
group. Neither FPL 55712 nor A63162 significantly affected the increase. On the contrary, DMTU significantly attenuated the
increase in MDA during the recovery period. These results suggest that inhibition of LTs leads to suppression at SP levels
and HIB, whereas DMTU attenuates HIB by means of other mechanisms.
Accepted for publication: 25 April 2000 相似文献
12.
13.
E. N. Schachter E. Zuskin N. Rienzi S. Goswami S. Maayani A. E. Wan V. Castranova P. Siegel M. Whitmer J. Mustajbegovic 《Lung》1998,176(1):35-44
The effect of paper dust collected at two different locations in a paper recycling plant (PD1 and PD2) on isolated nonsensitized
guinea pig tracheal smooth muscle was studied in vitro. Dust extracts were prepared as a 1:10 w/v aqueous solution. Dose-related
contractions of guinea pig tracheal rings were elicited with both PD1 and PD2. Pharmacologic studies were performed with atropine
(10−6 M), indometacin (10−6 M), pyrilamine (10−6 M), LY171883 (10−5 M), nordihydroguaiaretic acid (10−5 M), and TMB8 (10−5 M). The possible role of endogenous neuropeptides in this constrictor process was studied by depleting neural mediators with
capsaicin (5 × 10−6 M) before challenge with dust extracts. Constrictor effects were partially inhibited by a wide variety of the mediator blocking
agents. The effects of both extracts were almost totally inhibited by the anticholinergic agent atropine, suggesting that
a principal pathway mediating this response may involve the parasympathetic nervous system. The intracellular calcium-blocking
agent TMB8 also induced a reduction of the contractile responses to PD1 and PD2 concsistent with the well established role
of intracellular calcium in smooth muscle constriction. Pretreatment with capsaicin significantly increased the contractile
activity of paper dust extracts but only at the higher doses of these extracts. This suggests that the effect of paper dust
is not initiated by the release of mediators stored in sensory nerves but that the prerelease of these mediators may enhance
the constrictor effects of these dusts. We suggest that paper dust extracts cause dose-related airway smooth muscle constriction
possibly associated with the release of cholinergic as well as other mediators. The constrictor effect does not require tissue
presensitization or the release of neuropeptides from sensory nerves.
Accepted for publication: 21 March 1997 相似文献
14.
Effects of Age, Gender, Disease, and Multisystem Involvement on Oxygen Saturation Levels in Dysphagic Persons 总被引:2,自引:0,他引:2
Colodny N 《Dysphagia》2001,16(1):48-57
The purpose of this study was to examine the effects of age, gender, disease, and multisystem involvement on SpO2 levels of 104 dysphagic patients and 77 nondysphagic persons. Results indicated that solid aspirators had lower SpO2 levels than liquid aspirators, penetrators, and nondysphagics. In addition, SpO2 levels varied by age, with older persons having lower levels than younger persons among dysphagics but not among nondysphagics.
Patients with COPD had lower SpO2 levels than dysphagics with other disorders. Significant interactions were found among age, gender, and disease. Multisystem
involvement was found not to be a factor in SpO2 levels. It was concluded that although normal aging processes reduce swallowing and pulmonary functioning, it became a significant
factor only when combined with an assault to the system, such as CVA or COPD. 相似文献
15.
The Role of the Insular Cortex in Dysphagia 总被引:5,自引:0,他引:5
Recent data indicate that dysphagia may occur following unilateral cortical stroke; however, the elucidation of specific
cytoarchitectonic sites that produce deglutition disorders remains unclear. In a previous study of unilateral cortical stroke
patients with dysphagia, Daniels et al. [8] proposed that the insula may be important in swallowing as it was the most common
lesion site in the patients studied. Therefore, 4 unilateral stroke patients with discrete lesions of the insular cortex were
studied to further facilitate understanding of the role of the insula in swallowing. Dysphagia, as confirmed by videofluoroscopy,
was evident in 3 of the 4 patients; all had lesions that involved the anterior insula, whereas the only patient without dysphagia
had a lesion restricted to the posterior insula. These data suggest that the anterior insula may be an important cortical
substrate in swallowing. The anterior insula has connections to the primary and supplementary motor cortices, the ventroposterior
medial nucleus of the thalamus, and to the nucleus tractus solitarius, all of which are important regions in the mediation
of oropharyngeal swallowing. Therefore, discrete lesions of the anterior insula may disrupt these connections and, thereby,
produce dysphagia. 相似文献
16.
In seven alpha-chloralose anesthetized dogs we examined the contribution of lung afferents to the rapid, shallow breathing
induced by inhalation of 10 breaths of histamine aerosol. In four spontaneously breathing dogs, the inhalation of histamine
caused an increased respiratory frequency, decreased tidal volume, and decreased dynamic lung compliance. Selective blockade
of pulmonary C-fibers abolished a reflex-induced increase in respiratory frequency but did not significantly affect the reductions
in tidal volume or lung compliance. Terbutaline treatment in combination with C-fiber blockade abolished the reductions in
tidal volume and lung compliance induced by histamine. In three separate alpha-chloralose anesthetized, open-chest, mechanically
ventilated dogs, we recorded an increase in the inspiratory activity of rapidly adapting pulmonary stretch receptors (RARs)
induced by the inhalation of histamine aerosol. Selective C-fiber blockade abolished histamine-induced increases in RAR activity
while only partially attenuating reductions in lung compliance. We conclude that the increase in RAR activity induced by histamine
depends on intact C-fibers and not on a direct effect of histamine on RARs or an indirect effect of histamine reducing lung
compliance. In addition, our data illustrate the multiple interactions that occur between the various vagal afferents and
their roles in the reflexes induced by histamine inhalation.
Accepted for publication: 2 December 1999 相似文献
17.
Non-Invasive Estimation of Pulmonary Arterial Hypertension in Chronic Obstructive Pulmonary Disease 总被引:3,自引:0,他引:3
K. Spiropoulos N. Charokopos T. Petsas G. Trakada D. Dougenis A. Mazarakis J. Christodoulou A. Peristerakis P. Ginopoulos N. Mastronikolis D. Alexopoulos 《Lung》1999,177(2):65-75
The feasibility and reliability of the combination of several noninvasive methods using a multivariate method of analysis
to predict pulmonary artery hypertension (PAH) is evaluated in 20 patients with chronic obstructive pulmonary disease. These
methods comprised arterial blood gases (Pao
2, Paco
2), pulmonary functional parameters (FEV1), echo-Doppler parameters (tricuspid regurgitation jets, acceleration time on pulmonary valve), computed tomography measurements
(transhilar distance, hilar thoracic index, and measurement of the descending branch of the right pulmonary artery to the
lower lobe). A multiple stepwise regression analysis (including one Doppler parameter, two parameters of arterial blood gases,
and one functional parameter) revealed a coefficient of determination (R
2) equal to 0.954 for mean pulmonary artery pressure (MPAP) with a standard error of estimate (S.E.E.) of 5.25 mmHg. A stepwise
regression analysis including computed tomography and radiographic parameters revealed an R
2 equal to 0.970 for PAP with a S.E.E. of 4.26 mmHg. Logistical regression analysis classified correctly 80% of patients with
PAH using noninvasive methods such as the diameter of the main pulmonary artery and the diameter of the left pulmonary arterial
branch calculated by computed tomography. Not only the presence of PAH but also the level of MPAP can be estimated by the
combination of multiple stepwise and logistical regression analyses.
Accepted for publication: 13 August 1998 相似文献
18.
Angiotensin-converting Enzyme Activity by Canine Pulmonary Microvascular and Central Pulmonary Artery Endothelial Cells Exposed to Hypoxia 总被引:1,自引:0,他引:1
To compare the amount of angiotensin-converting enzyme (ACE) activity in pulmonary artery endothelial cells from different
sites and to examine the effect of severe hypoxia (less than 1% of O2 in 5% CO2 and 95% N2) on the ACE activity expressed by these cells, endothelial cells were harvested and cultured from canine main pulmonary artery
by scraping the luminal surface of the artery and from canine pulmonary artery microvessels by infusing chilled buffer with
microcarrier beads and 0.02% ethylenediamine tetraacetic acid (EDTA). ACE activity in cell lysates and culture medium was
evaluated by fluorometric assay with hippuryl-L-histidyl-L-leucine as a substrate.
ACE activity in cell lysates and postculture medium of pulmonary microvascular endothelial cells (PMVEC) was higher than in
cell lysates and culture medium of central pulmonary artery endothelial cells (PAEC). However, hypoxia suppressed cellular
ACE activity in both PAEC and PMVEC. The degree of suppression of ACE activity by hypoxia, which was determined as (ACE activity
in normoxia − ACE activity in hypoxia)/ACE activity in normoxia × 100(%), was larger in PMVEC than in PAEC.
The pulmonary microvasculature may be a greater source of ACE than central pulmonary artery, and the ACE activity of pulmonary
microvascular endothelial cells seem to be sensitive to hypoxia, although the small diameter of the vessels improves conditions
for interaction of blood-borne substance with endothelial enzymes.
Accepted for publication 10 July 2000 相似文献
19.
J. C. Thakker J.-Q. Xia D. A. Rickaby G. S. Krenz K. J. Kelly V. P. Kurup C. A. Dawson 《Lung》1999,177(2):89-100
Sensitization to latex proteins can cause immediate IgE mast cell-mediated reactions. Health care workers have been found
to be particularly at risk because of high exposure. Latex allergy can be produced in mice as demonstrated by IgE and eosinophil
responses. Thus the mouse is a potential animal model for studying this disease, but the airway response to latex sensitization
in mice has not been evaluated previously. In the present study, we immunized BALB/c mice intranasally with nonammoniated
latex proteins. Animals were anesthetized, and lung mechanics were evaluated plethysmographically. Changes in pulmonary conductance
(GL) and compliance (Cdyn) were measured in response to a nonspecific challenge with methacholine or to a direct challenge with intravenous latex antigen.
Latex sensitization resulted in elevated levels of IgE and latex-specific IgG1 as well as interstitial infiltrates consistent with an allergic response. The methacholine dose-response ED50 for GL was 116.4 μg for the control mice and fell significantly to 20.9 μg for latex-sensitized mice. The ED50 calculated for Cdyn was also significantly lower after latex sensitization. The GL in latex-sensitized mice challenged with latex antigen fell significantly from a prechallenge value of 1.87 ± 0.41 (S.E.)
to 0.198 ± 0.03 ml · s−1· cmH2O after latex antigen challenge. The results indicate that latex-sensitized mice did exhibit increased airway reactivity in
the methacholine challenge test. The latex allergic response in mice is unique in that direct challenge with latex antigen
itself also resulted in a significant airway response.
Accepted for publication: 10 September 1998 相似文献
20.
Effects of Halothane, Enflurane, Isoflurane, and Sevoflurane on Slowly Adapting Pulmonary Stretch Receptor Activity in Anesthetized Dogs 总被引:1,自引:0,他引:1
The aim of this study was to evaluate the effects of halothane, enflurane, isoflurane, and sevoflurane on slowly adapting
pulmonary stretch receptor (SAR) activity in dogs. Eight beagles were anesthetized with an intravenous injection of a mixture
of urethane and α-chloralose as a basal anesthesia, then vagotomized, artificially ventilated, and chest opened. Single afferent
activities from SARs were recorded from the peripheral nerve cut end of the left vagus. Changes in SAR activities with inhalation
of halothane, enflurane, isoflurane, and sevoflurane at 1, 1.5, and 2 times the minimal alveolar anesthetic concentration
(MAC) were measured, and differences in the discharges within and among four anesthetics were evaluated. As a result, two
different types of SARs, low threshold SARs and high threshold SARs, were detected in this study. In all anesthetics, expiratory
discharges of low threshold SARs decreased significantly in a dose-dependent manner, whereas inspiratory discharges did not
change significantly at any anesthetic level. Discharges of high threshold SARs tended to decrease with increasing anesthetic
level; however, no statistical significance was observed at any anesthetic level. Only one exception to these changes was
observed at 1 MAC of halothane where no significant decrease in the expiratory discharge of low threshold SARs or significant
increase in the discharge of high threshold SARs was induced against a control value. In conclusion, recent inhalation anesthetics,
except for halothane at the light anesthetic level, tended to decrease SAR activities depending on the anesthetic level, suggesting
attenuation of the Hering-Breuer inflation reflex. 相似文献