scholarly journals Extravascular Lung Water and Acute Lung Injury

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Ritesh Maharaj
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Extravascular Lung Water ◽  
Response To Treatment ◽  
Dilution Method ◽  
Lung Water ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Chest Auscultation

Acute lung injury carries a high burden of morbidity and mortality and is characterised by nonhydrostatic pulmonary oedema. The aim of this paper is to highlight the role of accurate quantification of extravascular lung water in diagnosis, management, and prognosis in “acute lung injury” and “acute respiratory distress syndrome”. Several studies have verified the accuracy of both the single and the double transpulmonary thermal indicator techniques. Both experimental and clinical studies were searched in PUBMED using the term “extravascular lung water” and “acute lung injury”. Extravascular lung water measurement offers information not otherwise available by other methods such as chest radiography, arterial blood gas, and chest auscultation at the bedside. Recent data have highlighted the role of extravascular lung water in response to treatment to guide fluid therapy and ventilator strategies. The quantification of extravascular lung water may predict mortality and multiorgan dysfunction. The limitations of the dilution method are also discussed.

scholarly journals Management of Phosgene-Induced Acute Lung Injury (ALI) by Personalized Protective PEEP-ECMO: What Can We Learn from Animal Bioassays?

2019 ◽  
pp. 1-9
Author(s):  
Chunli Yang ◽  
Chunli Yang ◽  
Yang Xiaogang ◽  
Zhaohui He
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Dead Space ◽  
Extravascular Lung Water ◽  
Lung Mechanics ◽  
Lung Edema ◽  
Lung Water ◽  
Extravascular Lung Water Index ◽  
Water Index ◽  
Arterial Blood

Background: Phosgene (carbonyl dichloride) gas is an indispensable chemical intermediate used in numerous industrial processes. Acute lung injury (ALI) caused by accidental inhalation exposure to phosgene is characterized pulmonary edema being phenotypically manifested after an asymptomatic or more precisely phrased “clinical occult” period. Opposite to common clinical practice, protective treatment should be given preference to curative treatment. Treatment initiated already during the asymptomatic phase shortly after exposure requires prognostic endpoints preceding the lung edema for triage and re-triage. Treatment strategies need to be personalized and exposure-dose related. The objective of this post-hoc analysis of published data is to assess prognostic value of ventilation dead-space (Vd/Vt) and extravascular lung water index (EVLWI) to guide treatment by protective PEEP supplemented by venovenous (vv) ECMO. Methods: This paper aims to compare the overarching published framework from systematic toxicological research of phosgene in animal bioassays with the clinical evidence from four accidentally phosgenepoisoned workers admitted to hospital with life-threatening lung edema. Treatment focused on a combination of protective PEEP and ECMO to reverse phosgene-induced deterioration in lung mechanics by personalized mechanical ventilation. Endpoints selected for titration PEEP focused on endpoints indicative of decoupling cardiopulmonary and vascular functions. To better understand any cardiogenic and vascular disturbances, titration endpoints included calculated ventilation dead-space (Vd/Vt), measured extravascular lung water index (EVLWI), arterial blood gases and acid-base status, systemic vascular resistance index (SVRI), and cardiac index (CI). EVLWI and APACHE II criteria guided the course of treatment in adjusting plateau pressure (Pplat), positive end-expiratory pressure (PEEP), and driving pressure (ΔP). Results: Remarkable equivalence of human data and those from controlled inhalation studies with phosgene on rats and dogs was found. The endpoint of choice guiding PEEP ventilation and implementation of ECMO was EVLWI. This maker of lung edema precisely reflects the increased wet lung weights in animals. Conclusions: ECMO-supplemented PEEP not only mitigates hypoxemia at conditions of severe ARDS and it also provides a means to reduce driving and plateau pressures minimizing ventilatorassociated lung injury.

scholarly journals Effect of Recruitment and Body Positioning on Lung Volume and Oxygenation in Acute Lung Injury Model

2008 ◽  
Vol 36 (6) ◽  
pp. 792-797 ◽  
Author(s):  
H. G. Ryu ◽  
J.-H. Bahk ◽  
H.-J. Lee ◽  
J.-G. Im
Keyword(s):  
Acute Lung Injury ◽  
Oleic Acid ◽  
Lung Injury ◽  
Lung Volume ◽  
Supine Position ◽  
Recruitment Manoeuvre ◽  
Prone Positioning ◽  
Dependent Lung ◽  
Arterial Blood Gas ◽  
Arterial Blood

The mechanism of oxygenation improvement after recruitment manoeuvres or prone positioning in acute lung injury or acute respiratory distress syndrome is still unclear. We tried to determine the mechanism responsible for the effects of recruitment manoeuvres or prone positioning on lung aeration using a whole lung computed tomography scan in an oleic acid induced acute lung injury canine model. Twelve adult mongrel dogs were allocated into either the supine group (n=6) or the prone group (n = 6). After the establishment of acute lung injury, three recruitment manoeuvres were performed at one-hour intervals. Haemodynamic and ventilatory variables, arterial blood gas analyses and CT scans of the whole lung were obtained 90 minutes after oleic acid injection and five minutes before and after each recruitment manoeuvre. Recruitment manoeuvres in the supine position improved oxygenation (P=0.025) that correlated with increase of the poorly- and well-aerated dorsal (dependent) lung volume (r=0.436, P=0.016). Prone positioning increased oxygenation (P=0.004) that also correlated with increase of the poorly- and well-aerated dorsal (nondependent) lung volume (r=0.787, P <0.001). However, the recruitment manoeuvre in the prone position had no effect on oxygenation despite an increase in ventral (dependent) lung volume. The increase in PO2 after recruitment manoeuvres in the supine position or after prone positioning is related to the increase of the poorly- and well-aerated dorsal lung.

Low-dose PGI2 prevents monocrotaline-induced thromboxane production and lung injury

1986 ◽  
Vol 60 (2) ◽  
pp. 464-471 ◽  
Author(s):  
G. T. Czer ◽  
J. Marsh ◽  
R. Konopka ◽  
K. M. Moser
Keyword(s):  
Pulmonary Hypertension ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Platelet Activation ◽  
Endothelial Damage ◽  
Base Line ◽  
Lung Water ◽  
Platelet Deposition ◽  
Thromboxane Production

In animals, monocrotaline induces an acute lung injury secondary to capillary endothelial damage. To date, no reports have appeared dealing with the role of prostaglandins in monocrotaline-induced injury. Our studies, in dogs, revealed that monocrotaline (30 mg/kg iv) caused an acute and persistent thrombocytopenia, lung platelet deposition, pulmonary hypertension, and increased extravascular lung water (EVLW). The pulmonary hypertensive response was biphasic. Thromboxane B2 levels were similarly biphasic, peaking at 5 min and 2 h. The levels of 6-keto-PGF1 alpha peaked at 30 min and returned to base line at 3 h. Pulmonary vascular resistance paralleled thromboxane levels. Infusion of prostacyclin (PGI2) at 50 ng X kg-1 X min-1 effectively prevented the thrombocytopenia, lung platelet deposition, pulmonary hypertension, and increased EVLW; and it decreased excess thromboxane production by 79%. These results suggest that platelet activation and lung sequestration play a role in acute lung injury due to monocrotaline, and that the resultant thromboxane production may contribute to the pulmonary hypertension. PGI2 ameliorates monocrotaline-induced injury, perhaps by preventing platelet activation.

scholarly journals Somatostatin Reduces the Acute Lung Injury of Mice via Increasing the Affinity of Glucocorticoid Receptor

2016 ◽  
Vol 38 (4) ◽  
pp. 1354-1364 ◽  
Author(s):  
Yan Zhao ◽  
Min Zhang ◽  
Ren-Ping Xiong ◽  
Xing-Yun Chen ◽  
Ping Li ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Glucocorticoid Receptor ◽  
Binding Capacity ◽  
Blood Gases ◽  
Protective Role ◽  
Lung Water ◽  
Beneficial Effects ◽  
Arterial Blood ◽  
Lung Injuries

Background/Aims: Although it has been reported that somatostatin (SOM) upregulated the level of 90-kD heat shock protein (Hsp90), which participates in the inflammatory regulation by its client proteins, such as glucocorticoid receptor (GR), it remains unclear if it has a protective role against acute lung injury (ALI). Methods: ALI model was established by the injection of oleic acid (OA) into the tail vein of mice. Lung injury was assessed by histological analysis, lung water content and arterial blood gases. The levels of Hsp90 and GR, the binding capacity and the affinity of GR were examined. Results: It was showed that pretreatment with SOM significantly increased Hsp90 levels and alleviated lung injuries in OA-injected mice. Furthermore, SOM increased the GR expression and improved the affinity of the GR in animals with lung injury. However, little alteration was found in the maximum binding capacity of the GR in mice with or without SOM. Conclusion: The data indicate SOM exerts a protective effect by increasing Hsp90 abundant and further enhancing the affinity of the GR. The beneficial effects of SOM treatment provide a new strategy for modulation of GR efficiency and alleviation of acute lung injury.

scholarly journals Peripheral Leukocytapheresis Attenuates Acute Lung Injury Induced by LipopolysaccharideIn Vivo

2012 ◽  
Vol 2012 ◽  
pp. 1-9
Author(s):  
Zhi-Gao He ◽  
Jian Huang ◽  
Shun-Gang Zhou ◽  
Jing He ◽  
Fang-Xiang Chen ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Distress Syndrome ◽  
Serum Levels ◽  
Partial Removal ◽  
Arterial Blood Gas ◽  
The Past ◽  
Arterial Blood ◽  
Lung Injuries ◽  
Elastase Level

The mortality of acute lung injury and acute respiratory distress syndrome (ALI/ARDS) remains high and efforts for prevention and treatments have shown little improvement over the past decades. The present study investigated the efficacy and mechanism of leukocytapheresis (LCAP) to partially eliminate peripheral neutrophils and attenuate lipopolysaccharide (LPS)-induced lung injury in dogs. A total of 24 healthy male mongrel dogs were enrolled and randomly divided into LPS, LCAP and LCAP-sham groups. All animals were injected with LPS to induce endotoxemia. The serum levels of leucocytes, neutrophil elastase, arterial blood gas, nuclear factor-kappa B (NF-κB) subunit p65 in lung tissues were measured. The histopathology and parenchyma apoptosis of lung tissues were examined. We found that 7, 3, and 7 animals in the LPS, LCAP, and sham-LCAP groups, respectively, developed ALI 36 h after LPS infusion. The levels of NF-κB p65 in lung tissue, neutrophils and elastase in blood, decreased significantly following LCAP. LCAP also alleviated apoptosis, and NF-κB p65 in lung tissues. Collectively, our results show that partial removal of leucocytes from peripheral blood decreases elastase level in serum. This, in turn, attenuates lung injuries and may potentially decrease the incidence of ALI.

scholarly journals Bone Marrow Mesenchymal Stem Cells Ameliorates Seawater-Exposure-Induced Acute Lung Injury by Inhibiting Autophagy in Lung Tissue

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Qiu-ping Liu ◽  
Dang-xia Zhou ◽  
Li Sun ◽  
Luo Ling ◽  
Chang-gui Wu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Blood Gas ◽  
Lung Weight ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Marrow Mesenchymal Stem Cells

Seawater drowning can lead to acute lung injury (ALI). Several studies have shown that bone marrow mesenchymal stem cells (BMSC) treatment could attenuate ALI. However, the mechanisms underlying this phenomenon still remain elusive. Therefore, this study aimed to investigate whether BMSC treatment can ameliorate seawater-induced ALI and its underlying mechanisms in a rat model. In this study, arterial blood gas, lung weight coefficient, and TNF-α, and IL-8 in bronchoalveolar lavage fluid (BALF), as well as histopathology examination, were used to detect the lung injury of seawater exposure. Moreover, western blot and RT-PCR were used to explore autophagy in lung tissues. The results demonstrated that seawater exposure induced ALI including impaired arterial blood gas, pulmonary edema, histopathologic changes, and inflammatory response in lung tissues. What is more, these changes were partly ameliorated by BMSC treatment through inhibition of autophagy in lung tissues. The application of BMSC may be a potential effective treatment for seawater-induced ALI.

Ibuprofen reduces ethchlorvynol lung injury: possible role of blood flow distribution

1992 ◽  
Vol 72 (3) ◽  
pp. 1156-1165 ◽  
Author(s):  
K. Yagi ◽  
L. J. Baudendistel ◽  
T. E. Dahms
Keyword(s):  
Blood Flow ◽  
Lung Injury ◽  
Extravascular Lung Water ◽  
Gas Transfer ◽  
Venous Admixture ◽  
Lung Water ◽  
Edema Formation ◽  
Edema Fluid ◽  
Pretreated Group

The role of cyclooxygenase products in acute lung injury was determined by pretreatment of dogs with ibuprofen before injury with intravenous ethchlovynol (ECV). In animals given ECV only, lung injury resulted in extravascular lung water of 18.9 ml/kg after 2 h, which was significantly higher than the 14.8 ml/kg in the group pretreated with ibuprofen. The comparison of gravimetric and indicator-dilution measurements of edema fluid indicates that edema fluid could not be reliably detected after treatment with ibuprofen because of diversion of flow from injured areas. Venous admixture increased from 6% at baseline to 32% 120 min after ECV in the vehicle-pretreated group compared with an increase from 4% at baseline to 7% in the ibuprofen-pretreated group. The regression analysis of the relationship between venous admixture and extravascular lung water indicated that, at any level of edema, venous admixture was significantly less in the group treated with ibuprofen than in the untreated group. Measurement of plasma and bronchoalveolar lavage fluid indicated that ibuprofen inhibited cyclooxygenase activity without affecting lipoxygenase activity. These results suggest that in intact dogs ibuprofen has a protective effect on both pulmonary gas transfer and pulmonary edema formation in ECV-injured lungs, which is consistent with limiting blood flow to injured segments of the lung.

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