scholarly journals Non-respiratory functions of lungs in experimental intracerebral hemorage during fingolimod injection

2022 ◽  
Vol 20 (4) ◽  
pp. 70-74
Author(s):  
M. A. Urakova
Keyword(s):  
Reference Group ◽  
Lung Surfactant ◽  
Gravimetric Method ◽  
Stability Index ◽  
Correction Method ◽  
Immunosuppressive Drug ◽  
Lung Edema ◽  
Water Metabolism ◽  
Blood Filling ◽  
Major Surface

Introduction. Intracerebral hemorrhage (ICH) is frequently accompanied by respiratory system complications. One of the correction method of post stroke complications is administration of immunosuppressive drug fingolimod. Theobjective of the study is to investigate non-respiratory lung functions in experimental ICH during fingolimod treatment. Materials and methods. Animals were divided into 3 groups: group 1 with ICH, group 2 with ICH receiving fingolimod and group 3 as reference group. Intracranial hemorrhage was modelled by 160 μl autologic blood injection into lateral brain ventricle (P=0.6; D=1.5; V=3.5). Fingolimod (FTY 720, «Sigma») was administered within 1 hour after ICH (intraabdominal, 1 mg/kg). Biochemistry and functional parameters of the lung surfactant in animals were studied. Phospholipids fractions spectrum was assessed by thin-layer chromatography, superficial surfactant activity by Wilhelmi method. Parameters of water metabolism, pulmonary blood filling were studied by gravimetric method. Level of blood nitric oxide was estimated by amount of nitrates and nitrites stable terminal metabolites. Results. We revealed that experimental ICH causes a decrease of alveolar stability index by 9 %, decrease of total alveolar phospholipids content by 25 % and change of its fraction composition, i.e. decrease of major surface active fraction (phosphatidylcholine) by 68 %, increase of phosphatidic acid amount by 151 % and increase of lisophosphatidylcholine by 163 %. Besides that, experimental ICH is followed by lung edema on the lung blood filling background and increase of blood NO. Fingolimod administration does not affect surfactant surface activity but totally corrects water balance, lung blood filling and blood NO content.

scholarly journals A study on the development of a light scattering particulate matter sensor and monitoring system

2020 ◽  
Vol 17 (3) ◽  
pp. 867-890
Author(s):  
Jun-Hee Choi ◽  
Hyun-Sug Cho
Keyword(s):  
Big Data ◽  
Particulate Matter ◽  
Light Scattering ◽  
Real Time ◽  
Monitoring System ◽  
Low Cost ◽  
Gravimetric Method ◽  
Correction Method ◽  
Measurement Methods ◽  
Linear Correction

The gravimetric method, which is mainly used among particulate matter (PM) measurement methods, includes the disadvantages that it cannot measure PM in real time and it requires expensive equipment. To overcome these disadvantages, we have developed a light scattering type PM sensor that can be manufactured at low cost and can measure PM in real time. We have built a big data system that can systematically store and analyze the data collected through the developed sensor, as well as an environment where PM states can be monitored mobile in real time using such data. In addition, additional studies were conducted to analyze and correct the collected big data to overcome the problem of low accuracy, which is a disadvantage of the light scattering type PM sensor. We used a linear correction method and proceeded to adopt the most suitable value based on error and accuracy.

scholarly journals Inhibition of Prostaglandin F2α Receptors Exaggerates HCl-Induced Lung Inflammation in Mice

2021 ◽  
Vol 22 (23) ◽  
pp. 12843
Author(s):  
Toko Maehara ◽  
Ko Fujimori
Keyword(s):  
Umbilical Vein ◽  
Lung Surfactant ◽  
Neutrophil Migration ◽  
Prostaglandin F2α ◽  
Lavage Fluid ◽  
Clinical Feature ◽  
Lung Edema ◽  
Induced Expression ◽  
Respiratory Dysfunction

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are severe respiratory disorders that are caused by aspiration, sepsis, trauma, and pneumonia. A clinical feature of ALI/ARDS is the acute onset of severe hypoxemia, and the mortality rate, which is estimated at 38–50%, remains high. Although prostaglandins (PGs) are detected in the bronchoalveolar lavage fluid of patients with ALI/ARDS, the role of PGF2α in ALI remains unclear. We aimed to clarify the role of PGF2α/PGF2α receptor (FP) signaling in acid-induced ALI using an FP receptor antagonist, AL8810. Intratracheal injection of hydrochloric acid (HCl) increased neutrophil migration into the lungs, leading to respiratory dysfunction. Pre-administration of AL8810 further increased these features. Moreover, pre-treatment with AL8810 enhanced the HCl-induced expression of pro-inflammatory cytokines and neutrophil migratory factors in the lungs. Administration of HCl decreased the gene expression of lung surfactant proteins, which was further reduced by co-administration of AL8810. Administration of AL8810 also increased lung edema and reduced mRNA expression of epithelial sodium channel in the lungs, indicating that AL8810 reduced fluid clearance. Furthermore, AL8810 also increased lipopolysaccharide-induced expression of adhesion molecules such as intracellular adhesion molecule-1 and E-selectin in human umbilical vein endothelial cells. These results indicate that inhibition of FP receptors by AL8810 exacerbated HCl-induced ALI.

Early changes in lungs of rats exposed to 70 per cent O2

1975 ◽  
Vol 38 (1) ◽  
pp. 136-142 ◽  
Author(s):  
R. A. Redding ◽  
T. Arai ◽  
W. H. Douglas ◽  
H. Tsurutani ◽  
J. Overs
Keyword(s):  
Lung Surfactant ◽  
Weight Ratio ◽  
Lung Compliance ◽  
Lung Edema ◽  
Lung Weight ◽  
Morphological Alterations ◽  
Loop Area ◽  
Protein Contamination ◽  
Hysteresis Loop Area ◽  
Alveolar Capillary

Sixty-six respiratory disease-free rats, divided into four groups, were exposed to 70% O2 for 1.5, 4, 7, and 10 days and compared with 31 littermates exposed to room air for equal times. Lung surfactant was separated from macrophages and potential serum protein contamination by differential centrifugation of endobronchial washings. In the O2-exposed rats, developing lung edema was demonstrated by decreased dried/fresh lung weight ratio and increased alveolar protein content at 7 and 10 days. At 7 days, lung compliance slope and hysteresis loop area decreased, while critical opening pressure increased. Ultrastructurally, the only abnormality seen was an irregular widening of the alveolar capillary basement membrane on day 10. Alveolar lecithin content decreased slightly during the 10 days exposure, but remained highly saturated, whereas whole lung lecithin content increased. These results suggest that the initial mechanical and morphological alterations in rats exposed to 70% O2 are related to lung edema and are not dependent upon lung surfactant alterations.

Mitigation of pulmonary hyperoxic injury by administration of exogenous surfactant

1987 ◽  
Vol 62 (2) ◽  
pp. 756-761 ◽  
Author(s):  
S. Matalon ◽  
B. A. Holm ◽  
R. H. Notter
Keyword(s):  
Lung Injury ◽  
Lung Surfactant ◽  
Dry Weight ◽  
Exogenous Surfactant ◽  
Lung Edema ◽  
Lung Capacity ◽  
O2 Partial Pressure ◽  
Hyperoxic Lung Injury ◽  
Wet Weight ◽  
Severe Lung

We studied the effects of surfactant supplementation on the progression of lung injury in rabbits exposed to 100% O2 for 64 h and returned to room air for 24 h. At this time, rabbits not treated with surfactant exhibit a severe lung injury with hypoxemia, increased alveolar premeability to solute, decreased total lung capacity (TLC) and lung edema. For surfactant treatment, 125 mg of calf lung surfactant extract (CLSE), suspended in 6–8 ml of normal saline, were instilled intratracheally at 0 and 12 h posthyperoxic exposure. At 24 h postexposure, these CLSE-treated rabbits compared with saline controls had significantly higher amounts of lung phospolipids (34 +/- 4 vs. 4.5 +/- 0.6 mumol/kg body wt) and increased TLC (42 +/- 2 vs. 27 +/- 1 ml/kg), with significantly lower amounts of alveolar protein (36 +/- 3 vs. 56 +/- 3 mg/kg) and decreased lung wet weight-to-dry weight ratios (5.6 +/- 0.1 vs. 6.3 +/- 0.3). Surfactant supplementation also decreased the degree of lung atelectasis as reflected by the increase in arterial O2 partial pressure (PaO2) after breathing 100% O2 for 20 min (PaO2 = 460 +/- 31 vs. 197 +/- 52 Torr). These findings indicate that instillation of exogenous surfactant mitigates the progression of hyperoxic lung injury in rabbits.

The Clinical, Roentgenological and Morphological Effects of an Acute Exposure of Phosgene on the Lungs of Dogs

1971 ◽  
Vol 29 ◽  
pp. 236-237
Author(s):  
R. F. Bils ◽  
W. F. Diller ◽  
F. Huth
Keyword(s):  
Latent Period ◽  
Chemical Industry ◽  
Toxic Substance ◽  
Lung Edema ◽  
X Rays ◽  
Beagle Dogs ◽  
Male And Female ◽  
Morphological Alterations ◽  
Before And After ◽  
Electron Microscopes

Phosgene still plays an important role as a toxic substance in the chemical industry. Thiess (1968) recently reported observations on numerous cases of phosgene poisoning. A serious difficulty in the clinical handling of phosgene poisoning cases is a relatively long latent period, up to 12 hours, with no obvious signs of severity. At about 12 hours heavy lung edema appears suddenly, however changes can be seen in routine X-rays taken after only a few hours' exposure (Diller et al., 1969). This study was undertaken to correlate these early changes seen by the roengenologist with morphological alterations in the lungs seen in the'light and electron microscopes.Forty-two adult male and female Beagle dogs were selected for these exposure experiments. Treated animals were exposed to 94.5-107-5 ppm phosgene for 10 min. in a 15 m3 chamber. Roentgenograms were made of the thorax of each animal before and after exposure, up to 24 hrs.

Ultrastructure of bronchopulmonary lavage cells from bovines administered 3-methylindole: II. 24 hours post-treatment

1984 ◽  
Vol 42 ◽  
pp. 202-203
Author(s):  
Amreek Singh ◽  
Judith M. McLaren ◽  
Onkar S. Atwal ◽  
Peter Eyre
Keyword(s):  
Plasma Cells ◽  
Ciliated Cell ◽  
Lavage Fluid ◽  
Treated Group ◽  
Post Treatment ◽  
Lung Edema ◽  
Ciliated Cells ◽  
Thin Sections ◽  
Variable Diameter ◽  
Cell Pellet

Introduction3-methylindole (MI), a rumen metabolite of the amino acid L-tryptophan, has been shown to produce bovine pulmonary edema and emphysema. The airways contain free and exfoliated cells. A morphologic analysis of these cells may complement the understanding of the mechanism of lung edema. Ultrastructure of the bronchopulmonary lavage (BL) cells 24 h following MI oral administration to calves is described in this experiment. The 12 hours post-treatment results were described earlier.Materials and MethodsTwo Holstein-Friesian calves were each administered an oral dose of 0.2 g MI/Kg body weight and another two calves served as controls. The animals were euthanized with sodium pentabarbitol 24 h after receiving the compound. The lungs and trachea were removed and 0.1 M sodium phosphate buffered saline was infused into the lungs through the trachea. Glutaraldehyde fixative was added to the recovered BL fluid so as to form a 1% solution. The fluid was centrifuged and the resulting cell pellet was suspended in the buffer. The procedures were repeated on the suspension; the pellet was post-fixed in osmium tetroxide and was processed by conventional methods of section preparations for TEM examination. Lung samples from caudal lobes were fixed in 1.5% glutaraldehyde to obtain tissue sections for TEM.Results and DiscussionPulmonary alveolar macrophages (AM), neutrophils, ciliated epithelial cells, globule leukocytes and plasma cells were recovered from the BL fluid of the control and Mi-administered calves. Ciliated cells and globule leukocytes could not be harvested from the controls. The AM obtained from the treated calves (Fig. 1) in comparison with similar cells from the controls were larger, and contained large membrane-limited inclusions (phagolysosomes). There was a remarkable similarity between the lavaged AM and the AM studied in thin sections of lung (cf. Fig. 1 and Fig. 2). The neutrophil was the second most abundant cell type retrieved from the lavage fluid from the calves of control or treated group. Except for scanty pseudopodia in the neutrophils obtained from the Mi-receiving calves, the cells appeared unaltered (Fig. 3). Ciliated cells were abundant in the BL fluid of Mi-ingesting calves. A heterogeneous collection of vesicles filled the ciliated cell cytoplasm (Fig. 3). Globule leukocytes were commonly observed among BL cells of treated calves. The globule leukocytes were ca. 15 μm in diameter and contained round or elliptical nuclei with conspicuous nucleoli. The cytoplasmic granules, which are a prominent feature of globule leukocytes, were electron-opaque and had a variable diameter (0.5-3.0 μm). A one-line account of globule leukocytes in the bronchi of steers administered MI has appeared. Plasma cells were rare. Ultrastructure of BL cells is compatible with their response to chemical insult by MI.

Learned Placebo Effects in the Immune System

2014 ◽  
Vol 222 (3) ◽  
pp. 148-153 ◽  
Author(s):  
Sabine Vits ◽  
Manfred Schedlowski
Keyword(s):  
Nervous System ◽  
Immune System ◽  
Associative Learning ◽  
Placebo Response ◽  
Immunosuppressive Drug ◽  
Immune Functions ◽  
Placebo Effects ◽  
New Therapeutic Approaches ◽  
Biological Variables ◽  
Experimental Approaches

Associative learning processes are one of the major neuropsychological mechanisms steering the placebo response in different physiological systems and end organ functions. Learned placebo effects on immune functions are based on the bidirectional communication between the central nervous system (CNS) and the peripheral immune system. Based on this “hardware,” experimental evidence in animals and humans showed that humoral and cellular immune functions can be affected by behavioral conditioning processes. We will first highlight and summarize data documenting the variety of experimental approaches conditioning protocols employed, affecting different immunological functions by associative learning. Taking a well-established paradigm employing a conditioned taste aversion model in rats with the immunosuppressive drug cyclosporine A (CsA) as an unconditioned stimulus (US) as an example, we will then summarize the efferent and afferent communication pathways as well as central processes activated during a learned immunosuppression. In addition, the potential clinical relevance of learned placebo effects on the outcome of immune-related diseases has been demonstrated in a number of different clinical conditions in rodents. More importantly, the learned immunosuppression is not restricted to experimental animals but can be also induced in humans. These data so far show that (i) behavioral conditioned immunosuppression is not limited to a single event but can be reproduced over time, (ii) immunosuppression cannot be induced by mere expectation, (iii) psychological and biological variables can be identified as predictors for this learned immunosuppression. Together with experimental approaches employing a placebo-controlled dose reduction these data provide a basis for new therapeutic approaches to the treatment of diseases where a suppression of immune functions is required via modulation of nervous system-immune system communication by learned placebo effects.

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