Aerosol deposition and dispersion characterize lung injury in a canine model of emphysema

1995 ◽  
Vol 78 (4) ◽  
pp. 1585-1595 ◽  
Author(s):  
F. S. Rosenthal
Keyword(s):  
Lung Injury ◽  
Flow Rate ◽  
Aerosol Deposition ◽  
Canine Model ◽  
Lung Damage ◽  
Lung Mechanics ◽  
Breath Hold ◽  
Specific Marker ◽  
Air Space ◽  
Before And After

The deposition and dispersion of inhaled aerosol boluses were investigated as markers of lung injury in three dogs before and after emphysema was induced by papain exposure. After the experiments, lung damage was assessed histologically. Four unexposed dogs were used as controls. Effective air space diameter (EAD) was determined from aerosol deposition during a 5-s breath hold. Nonuniform ventilation was assessed from the spreading of the expired bolus, quantified as a coefficient of dispersion (CD), and from expired bolus skewness (SK). Experiments were done with a range of bolus penetrations and ventilatory flow rates. After papain exposure, EAD measured with the most penetrating boluses increased an average of 89% (P < 0.0001); CD and SK measured with boluses of medium penetration and a flow rate of 0.5 l/s increased an average of 24% (P < 0.02) and 98% (P < 0.002), respectively. The effects of lung injury on CD and SK increased with flow rate. Lung injury was confirmed by changes in lung mechanics and by histology. EAD measured with deeply penetrating boluses correlated significantly with the mean chord length measured morphometrically (P < 0.05). No correlation was found with more shallow boluses. The results indicate that EAD, CD, and SK are sensitive markers of lung injury in experimental emphysema and that EAD is a specific marker of increased air space size.

scholarly journals Effect of gravity on aerosol dispersion and deposition in the human lung after periods of breath holding

2000 ◽  
Vol 89 (5) ◽  
pp. 1787-1792 ◽  
Author(s):  
Chantal Darquenne ◽  
Manuel Paiva ◽  
G. Kim Prisk
Keyword(s):  
Flow Rate ◽  
Turbulent Mixing ◽  
Direct Evidence ◽  
Human Lung ◽  
Hold Time ◽  
Aerosol Deposition ◽  
Breath Holding ◽  
Breath Hold ◽  
Constant Flow Rate ◽  
Aerosol Dispersion

To determine the extent of the role that gravity plays in dispersion and deposition during breath holds, we performed aerosol bolus inhalations of 1-μm-diameter particles followed by breath holds of various lengths on four subjects on the ground (1G) and during short periods of microgravity (μG). Boluses of ∼70 ml were inhaled to penetration volumes (Vp) of 150 and 500 ml, at a constant flow rate of ∼0.45 l/s. Aerosol concentration and flow rate were continuously measured at the mouth. Aerosol deposition and dispersion were calculated from these data. Deposition was independent of breath-hold time at both Vp in μG, whereas, in 1G, deposition increased with increasing breath hold time. At Vp = 150 ml, dispersion was similar at both gravity levels and increased with breath hold time. At Vp = 500 ml, dispersion in 1G was always significantly higher than in μG. The data provide direct evidence that gravitational sedimentation is the main mechanism of deposition and dispersion during breath holds. The data also suggest that cardiogenic mixing and turbulent mixing contribute to deposition and dispersion at shallow Vp.

scholarly journals Sports-related lung injury during breath-hold diving

2016 ◽  
Vol 25 (142) ◽  
pp. 506-512 ◽  
Author(s):  
Tanja Mijacika ◽  
Zeljko Dujic
Keyword(s):  
Lung Injury ◽  
Lung Damage ◽  
Strenuous Exercise ◽  
Alveolar Haemorrhage ◽  
Breath Holding ◽  
Breath Hold ◽  
Pulmonary Barotrauma ◽  
Large Populations ◽  
Acute And Chronic Effects

The number of people practising recreational breath-hold diving is constantly growing, thereby increasing the need for knowledge of the acute and chronic effects such a sport could have on the health of participants. Breath-hold diving is potentially dangerous, mainly because of associated extreme environmental factors such as increased hydrostatic pressure, hypoxia, hypercapnia, hypothermia and strenuous exercise.In this article we focus on the effects of breath-hold diving on pulmonary function. Respiratory symptoms have been reported in almost 25% of breath-hold divers after repetitive diving sessions. Acutely, repetitive breath-hold diving may result in increased transpulmonary capillary pressure, leading to noncardiogenic oedema and/or alveolar haemorrhage. Furthermore, during a breath-hold dive, the chest and lungs are compressed by the increasing pressure of water. Rapid changes in lung air volume during descent or ascent can result in a lung injury known as pulmonary barotrauma. Factors that may influence individual susceptibility to breath-hold diving-induced lung injury range from underlying pulmonary or cardiac dysfunction to genetic predisposition.According to the available data, breath-holding does not result in chronic lung injury. However, studies of large populations of breath-hold divers are necessary to firmly exclude long-term lung damage.

Dry air-induced constriction in lung periphery: a canine model of exercise-induced asthma

1985 ◽  
Vol 59 (6) ◽  
pp. 1986-1990 ◽  
Author(s):  
A. N. Freed ◽  
B. Bromberger-Barnea ◽  
H. A. Menkes
Keyword(s):  
Flow Rate ◽  
Exposure Period ◽  
Canine Model ◽  
Base Line ◽  
Dry Air ◽  
Peripheral Airways ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Lung Periphery ◽  
Exercise Induced

We studied the effects of the flow of dry air on collateral tone in the lung periphery. A bronchoscope was wedged in sublobar segments of anesthetized dogs, and measurements of collateral resistance (Rcs) were recorded before and after flow was increased from 200 to 2,000 ml/min for a 5-min period. Five minutes after exposure was completed, Rcs increased by an average of 117 +/- 25.2% (SE) over control. Maximum Rcs occurred 5 min after the challenge was concluded and required 48 +/- 10.5 min to return to base line. When flow rate was held constant and exposure period varied, Rcs increased with increased stimulus duration. With exposure times held constant, the response of the collateral system was positively associated with changes in stimulus strength (flow rate). No refractory period was observed with repetitive challenges. Finally, when dry air (delivered at 22 degrees C) and conditioned air (i.e., delivered at 28 degrees C; relative humidity = 80%) challenges were alternated in the same wedged segment, dry air produced a mean increase in Rcs of 93.2%, whereas challenge with warm moist air increased Rcs only 33.5%. Regardless of which challenge was presented first, dry air consistently produced a greater constrictor response. This response is similar to that observed in cold air- and exercise-induced asthma and indicates that the lung periphery in dogs, like larger airways in asthmatic subjects, has the potential to increase tone when exposed to dry air. Peripheral airways in dogs thus constitute a model that can be used for the investigation of exercise-induced asthma.

Assessment of papain-induced lung injury in isolated lungs by measurements of aerosol deposition and mixing

1992 ◽  
Vol 72 (2) ◽  
pp. 459-467 ◽  
Author(s):  
F. S. Rosenthal ◽  
S. Wright
Keyword(s):  
Lung Injury ◽  
Regional Distribution ◽  
Aerosol Deposition ◽  
Breath Hold ◽  
Exposure Group ◽  
High Exposure ◽  
The Difference ◽  
Low Exposure ◽  
High Doses ◽  
Isolated Lungs

Aerosol bolus inspirations were used to assess lung injury in 15 isolated dog lungs exposed to low (0–375 units) or high doses (600–1,200 units) of papain. Effective air space size (EAD) was determined from aerosol deposition during a 5-s breath hold. Convective mixing was assessed by the spreading of the expired bolus with respect to expired volume, quantified by a coefficient of dispersion (CD) equal to the square root of the difference in the variances of the expired and inspired boluses divided by the volumetric penetration of the bolus. After exposure, CD measured with deeply penetrating boluses increased by an average of 2.5% in the low-exposure group (P greater than 0.05) and 28.0% in the high-exposure group (P less than 0.0001). CD measured with shallowly penetrating boluses decreased by 4.3% (P less than 0.0001) in the low-exposure group and increased by an average of 18.3% in the high-exposure group (P less than 0.05). Papain exposure caused EAD to increase in some lungs and decrease in others. For deep bolus penetrations, EAD changed by an average of -0.8% in the low-exposure group (P greater than 0.05) and +21.1% in the high-exposure group (P greater than 0.05). Both EAD and CD appeared to be sensitive to lung injury. However, changes in EAD were less consistent than those in CD, possibly due to changes caused by lung injury in the regional distribution of inspired aerosol.

Aerosol probes of lung injury in a 28-wk longitudinal study of mild experimental emphysema in dogs

1999 ◽  
Vol 86 (2) ◽  
pp. 725-731 ◽  
Author(s):  
Frank S. Rosenthal
Keyword(s):  
Lung Injury ◽  
Total Lung Capacity ◽  
Lung Mechanics ◽  
Partial Recovery ◽  
Lung Capacity ◽  
Air Space ◽  
Aerosol Dispersion ◽  
Increasing Trends ◽  
Experimental Emphysema

After baseline measurements of lung mechanics, effective air space diameter (EAD), and aerosol dispersion (AD), three dogs were exposed to two treatments of aerosolized papain (3 ml of a 4% solution), and measurements were repeated during a 28-wk follow-up period. EAD and AD were measured with boluses of 0.7-μm particles of di-2-ethylhexl sebacate, with Pen (i.e., volumetric bolus penetration/total lung capacity) between 0.1 and 0.4. After papain exposure, EAD increased a mean of 28% ( P < 0.0001) and AD (Pen = 0.3, 0.4) increased 4–7% ( P < 0.03). The progression of injury was indicated by increasing trends in total lung capacity ( P < 0.05), residual volume ( P < 0.05), and EAD ( P = 0.06) through week 18. There was no evidence of disease progression between weeks 18and 28, whereas some of the data for individual dogs suggested partial recovery from lung injury at week 28. The results show that aerosol probes can detect and characterize mild lung injury in experimental emphysema.

Intravenous Lidocaine Attenuates Acute Lung Injury Induced by Hydrochloric Acid Aspiration in Rabbits 

1998 ◽  
Vol 88 (5) ◽  
pp. 1300-1309 ◽  
Author(s):  
Kahoru Nishina ◽  
Katsuya Mikawa ◽  
Yumiko Takao ◽  
Makoto Shiga ◽  
Nobuhiro Maekawa ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Hydrochloric Acid ◽  
Lung Injury ◽  
Weight Ratio ◽  
The Other ◽  
Lung Damage ◽  
Lung Mechanics ◽  
Intravenous Lidocaine ◽  
Superoxide Anion Production ◽  
Acid Aspiration

Background Neutrophils play a crucial role in the pathogenesis of acid-induced acute lung injury. Lidocaine inhibits the function of neutrophils. This study aimed to determine whether lidocaine attenuates acute lung injury induced by hydrochloric acid (HCl) instillation. Methods In study 1, rabbits were divided into four groups (n = 7 each). Lung injury was induced by intratracheal HCl (0.1 N, 3 ml/kg) in two groups. The other two groups received saline intratracheally. Lidocaine given intravenously (2 mg/ g bolus + 2 mg x kg(-1) x h(-1) infusion) was started 10 min before intratracheal instillation in one HCl and one saline group, and saline was given intravenously in the other two groups. In study 2, rabbits (four groups of seven animals each) received HCl (0.1 N, 3 ml/kg) intratracheally. Treatment with intravenous lidocaine was started 10 min before, 10 min after, or 30 min after acid instillation, or saline was given intravenously 10 min before instillation. Results In study 1, HCl caused deterioration of the partial pressure of oxygen (PaO2), lung leukosequestration, decreased lung compliance, and increased the lung wet-to-dry weight ratio and albumin, interleukin-6 (IL-6), and IL-8 levels in bronchoalveolar lavage fluid. Lidocaine pretreatment attenuated these changes. Hydrochloric acid increased superoxide anion production by neutrophils and caused morphologic lung damage, both of which were lessened by lidocaine. In study 2, lidocaine given 10 min after acid instillation was as effective as pretreatment in PaO2, lung mechanics, and histologic examination. However, PaO2 changes in lidocaine 30 min after injury were similar to those in saline given intravenously. Conclusions Intravenous lidocaine started before and immediately after acid instillation attenuated the acute lung injury, in part by inhibiting the sequestration and activation of neutrophils.

Does Early Posttreatment with Lidocaine Attenuate Endotoxin-induced Acute Lung Injury in Rabbits?

1995 ◽  
Vol 83 (1) ◽  
pp. 169-177. ◽  
Author(s):  
Kahoru Nishina ◽  
Katsuya Mikawa ◽  
Nobuhiro Maekawa ◽  
Yumiko Takao ◽  
Hidefumi Obara
Keyword(s):  
Acute Lung Injury ◽  
Treatment Group ◽  
Lung Injury ◽  
Weight Ratio ◽  
Lung Damage ◽  
Lung Mechanics ◽  
Lung Edema ◽  
Platelet Counts ◽  
Peripheral Leukocyte ◽  
Cell Counts

Background It is well known that endotoxin causes acute lung injury, resulting in adult respiratory distress syndrome. Lidocaine pretreatment has recently been shown to attenuate endotoxin-induced lung injury in rabbits. The aim of the current study was to determine whether early postinjury treatment with intravenous lidocaine could attenuate acute lung injury induced by endotoxin in rabbits. Methods Thirty-two male anesthetized rabbits were randomly assigned to receive one of four treatments (n = 8 for each group): infusion of saline (group S-S), infusion of saline with lidocaine treatment (group S-L), infusion of Escherichia coli endotoxin (100 micrograms.kg-1 over a 60-min period) without lidocaine treatment (group E-S), or infusion of endotoxin with lidocaine treatment (group E-L). Ten minutes after the end of infusion of endotoxin (groups E-L and E-S) or saline (groups S-S and S-L), the animals received a bolus injection followed by continuous infusion of lidocaine (2 mg.kg-1 + 2 mg.kg-1.h-1 in groups S-L and E-L) or saline (groups S-S and E-S). The rabbits' lungs were ventilated with 40% O2. Hemodynamics, peripheral leukocyte and platelet counts, and arterial O2 tension (PaO2) were recorded during the ventilation period (6 h). After the observation, lung mechanics; the cell fraction of bronchoalveolar lavage fluid (BALF); and concentrations of activated complement components C3a and C5a, cytokines, and arachidonic acid metabolites in BALF were measured and analyzed. The ratio of lung wet weight to dry weight (W/D weight ratio) and albumin concentrations in BALF were analyzed as indexes of pulmonary edema. The Cypridina luciferin analogue-dependent chemiluminescence (representing O2 production) by neutrophils isolated from the pulmonary artery and light-microscopic findings of the lung were compared among the four groups. Results Endotoxin caused decreases in peripheral leukocyte and platelet counts, lung compliance, and PaO2. It caused increases in lung W/D weight ratio; polymorphonuclear cell counts in BALF; and albumin, C3a, C5a, tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-6, IL-8, and thromboxane B2 concentrations in BALF. Lidocaine attenuated the changes in W/D weight ratio and morphologic lung damage. The change in compliance, decrease in PaO2, and albumin concentrations in BALF were slightly but significantly less in rabbits receiving lidocaine after injury. The Cypridina luciferin analogue-dependent chemiluminescence by neutrophils was greater in rabbits receiving endotoxin without lidocaine than in those receiving endotoxin with lidocaine. Conclusions These results indicate that early treatment with lidocaine attenuates endotoxin-induced lung edema in rabbits without affecting chemical mediators in BALF. However, the improvement is slight and likely to be of little clinical significance.

scholarly journals Impaired Glucocorticoid Receptor Signaling Aggravates Lung Injury after Hemorrhagic Shock

Cells ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 112
Author(s):  
Jonathan M. Preuss ◽  
Ute Burret ◽  
Michael Gröger ◽  
Sandra Kress ◽  
Angelika Scheuerle ◽  
...  
Keyword(s):  
Intensive Care Unit ◽  
Lung Injury ◽  
Hemorrhagic Shock ◽  
Lung Tissue ◽  
Lung Inflammation ◽  
Lung Damage ◽  
Lung Mechanics ◽  
Cytokine Signaling ◽  
Pro Inflammatory Cytokines

We previously showed that attenuated lung injury after hemorrhagic shock (HS) coincided with enhanced levels of the glucocorticoid (GC) receptor (GR) in lung tissue of swine. Here, we investigated the effects of impaired GR signaling on the lung during resuscitated HS using a dysfunctional GR mouse model (GRdim/dim). In a mouse intensive care unit, HS led to impaired lung mechanics and aggravated lung inflammation in GRdim/dim mice compared to wildtype mice (GR+/+). After HS, high levels of the pro-inflammatory and pro-apoptotic transcription factor STAT1/pSTAT1 were found in lung samples from GRdim/dim mice. Lungs of GRdim/dim mice revealed apoptosis, most likely as consequence of reduced expression of the lung-protective Angpt1 compared to GR+/+ after HS. RNA-sequencing revealed increased expression of pro-apoptotic and cytokine-signaling associated genes in lung tissue of GRdim/dim mice. Furthermore, high levels of pro-inflammatory cytokines and iNOS were found in lungs of GRdim/dim mice. Our results indicate impaired repression of STAT1/pSTAT1 due to dysfunctional GR signaling in GRdim/dim mice, which leads to increased inflammation and apoptosis in the lungs. These data highlight the crucial role of functional GR signaling to attenuate HS-induced lung damage.

Pulmonary angiotensin-converting enzyme kinetics after acute lung injury in the rabbit

1988 ◽  
Vol 64 (6) ◽  
pp. 2508-2516 ◽  
Author(s):  
D. Riggs ◽  
A. M. Havill ◽  
B. R. Pitt ◽  
C. N. Gillis
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Angiotensin Converting Enzyme ◽  
Lung Damage ◽  
Converting Enzyme ◽  
Intratracheal Administration ◽  
Multiple Indicator Dilution ◽  
Before And After ◽  
High Doses

Depression of lung endothelial cell metabolic function may be an early and sensitive indicator of lung damage. When such functions are measured in vivo, substrates injected usually must be limited to "trace" doses due to the significant hemodynamic effects of high doses of substrate. Under first-order conditions (i.e., trace doses) the enzyme or transport system rate constant Vmax/Km may be calculated, but independent estimates of each variable (Vmax and Km) are not available. We therefore used multiple indicator-dilution methods and higher substrate concentrations to apply a mathematical model, based on saturable kinetics that yield independent estimates of the apparent kinetic parameters Vmax and Km for pulmonary angiotensin-converting enzyme (ACE). We used the ACE substrate, [3H]benzoyl-phenylalanyl-alanyl-proline ([3H]BPAP) and made these measurements and also estimates of serotonin [5-hydroxytryptamine (5-HT)] removal, before and after acute lung injury induced by intratracheal administration of phorbol myristate acetate (PMA). PMA significantly depressed the percent 5-HT removal (62 +/- 3 to 44 +/- 4%) and BPAP percent metabolism (74 +/- 2 to 66 +/- 2), when trace amounts of either compound were injected as a bolus.

scholarly journals Hot Box Investigations of a Ventilated Bioclimatic Wall for NZEB Building Façade

Energies ◽  
2021 ◽  
Vol 14 (5) ◽  
pp. 1327
Author(s):  
Dwinanto Sukamto ◽  
Monica Siroux ◽  
Francois Gloriant
Keyword(s):  
Energy Efficiency ◽  
Flow Rate ◽  
Experimental Setup ◽  
Air Flow Rate ◽  
Space Thickness ◽  
Zero Energy ◽  
Interior Space ◽  
Air Space ◽  
Thermal Metrology

The building sector is the largest consumer of energy, but there are still major scientific challenges in this field. The façade, being the interface between the exterior and interior space, plays a key role in the energy efficiency of a building. In this context, this paper focuses on a ventilated bioclimatic wall for nearly zero-energy buildings (NZEB). The aim of this study is to investigate an experimental setup based on a hot box for the characterization of the thermal performances of the ventilated wall. A specific ventilated prototype and an original thermal metrology are developed. This paper presents the ventilated prototype, the experimental setup, and the experimental results on the thermal performances of the ventilated wall. The influence of the air space thickness and the air flow rate on the thermal performances of the ventilated wall is studied.

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