High tidal volume mechanical ventilation with hyperoxia alters alveolar type II cell adhesion

2007 ◽  
Vol 293 (3) ◽  
pp. L769-L778 ◽  
Author(s):  
Leena P. Desai ◽  
Scott E. Sinclair ◽  
Kenneth E. Chapman ◽  
Aviv Hassid ◽  
Christopher M. Waters
Keyword(s):  
Mechanical Ventilation ◽  
Cell Adhesion ◽  
Tidal Volume ◽  
Focal Adhesion ◽  
Keratinocyte Growth Factor ◽  
Dominant Negative ◽  
High Tidal Volume ◽  
Alveolar Type ◽  
Type Ii ◽  
And Migration

Patients with acute respiratory distress syndrome undergoing mechanical ventilation may be exposed to both high levels of stretch and high levels of oxygen. We hypothesized that the combination of high stretch and hyperoxia promotes loss of epithelial adhesion and impairs epithelial repair mechanisms necessary for restoration of barrier function. We utilized a model of high tidal volume mechanical ventilation (25 ml/kg) with hyperoxia (50% O2) in rats to investigate alveolar type II (AT2) cell adhesion and focal adhesion signaling. AT2 cells isolated from rats exposed to hyperoxia and high tidal volume mechanical ventilation (MVHO) exhibited significantly decreased cell adhesion and reduction in phosphotyrosyl levels of focal adhesion kinase (FAK) and paxillin compared with control rats, rats exposed to hyperoxia without ventilation (HO), or rats ventilated with normoxia (MV). MV alone increased phosphorylation of p130Cas. RhoA activation was increased by MV, HO, and the combination of MV and HO. Treatment of MVHO cells with keratinocyte growth factor (KGF) for 1 h upon isolation reduced RhoA activity and restored attachment to control levels. Attachment and migration of control AT2 cells was significantly decreased by constitutively active RhoA or a kinase inactive form of FAK (FRNK), whereas expression of dominant negative RhoA in cells from MVHO-treated rats restored cell adhesion. Mechanical ventilation with hyperoxia promotes changes in focal adhesion proteins and RhoA in AT2 cells that may be deleterious for cell adhesion and migration.

Effects of Feedback and Education on Nurses’ Clinical Competence in Mechanical Ventilation and Accurate Tidal Volume Setting

2021 ◽  
Author(s):  
Samira Norouzrajabi ◽  
Shahrzad Ghiyasvandian ◽  
Alireza Jeddian ◽  
Ali Karimi Rozveh ◽  
Leila Sayadi
Keyword(s):  
Mechanical Ventilation ◽  
Body Weight ◽  
Tidal Volume ◽  
Clinical Competence ◽  
High Tidal Volume ◽  
Education Intervention ◽  
Predicted Body Weight ◽  
Post Test ◽  
The Mean ◽  
Effects Of Feedback

Background: Patients under mechanical ventilation are at risk of ventilator-associated complications. One of these complications is lung injury due to high tidal volume. Nurses’ competence in mechanical ventilation is critical for preventing ventilator-associated complications. This study assessed the effects of feedback and education on nurses’ clinical competence in mechanical ventilation and accurate tidal volume setting. Methods: This single arm pretest-post-test interventional study was conducted in 2019 at Shariati hospital affiliated to Tehran University of Medical Sciences. Participants were 75 conveniently selected nurses. Initially, nurses’ clinical competence in mechanical ventilation and ventilator parameters of 250 patients were assessed. A mechanical ventilation -based feedback and education intervention was implemented for nurses. Finally, mechanical ventilation clinical competence of nurses and ventilator parameters of 250 new patients were assessed. Moreover, patients’ height was estimated based on their ulna length and then, their predicted body weight was calculated using their estimated height. Accurate tidal volume was determined per predicted body weight.  Results: The mean score of nurses’ clinical competence increased from 8.27±3.09 at pretest to 10.07±3.34 at post-test (p<0.001). The mean values of both total tidal volume and tidal volume per kilogram of predicted body weight were significantly reduced respectively from 529.84±69.11 and 9.11±1.73 (ml) at pretest to 476.30±31.01 and 7.79±1.14 (ml) at post-test (p<0.001). Conclusion: The feedback and education intervention is effective in promoting nurses’ clinical competence in mechanical ventilation and reducing tidal volume. Thereby, it can reduce lung injuries associated with high tidal volume and ensure patient safety.

Keratinocyte growth factor increases mRNAs for SP-A and SP-B in adult rat alveolar type II cells in culture

1995 ◽  
Vol 269 (3) ◽  
pp. L344-L350 ◽  
Author(s):  
K. Sugahara ◽  
J. S. Rubin ◽  
R. J. Mason ◽  
E. L. Aronsen ◽  
J. M. Shannon
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Keratinocyte Growth Factor ◽  
Primary Cultures ◽  
Surfactant Proteins ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Adult Rat

The production of pulmonary surfactant, a complex of phospholipids and lung-specific surfactant proteins, is a primary function of alveolar type II cells. Although previous studies have demonstrated a role for cell-extracellular matrix interactions and normal cell shape in the maintenance of differentiated function in primary cultures of adult rat type II cells, a positive role for growth factors in surfactant protein gene expression in isolated normal adult type II cells has not been reported. In the present study, we have examined the effects of a panel of hormones, growth factors, and cytokines on the expression of mRNAs for surfactant proteins A, B, and C (SP-A, SP-B, and SP-C). Our results show that keratinocyte growth factor (KGF) induced a two- to threefold increase in steady-state levels of mRNAs for SP-A and SP-B, but had no effect on or decreased SP-C mRNA. The increase in SP-A mRNA was accompanied by an increase in SP-A protein. The effects of KGF were both dose and time dependent, and they could be neutralized by a monoclonal antibody against KGF. The effects of KGF were mimicked by acidic fibroblast growth factor, which will bind the KGF receptor. We conclude that KGF can support differentiation of alveolar type II cells as well as act as a mitogen, thus suggesting an important role for KGF in maintenance of the alveolar epithelium.

scholarly journals Effects of MMP-9 inhibition by doxycycline on proteome of lungs in high tidal volume mechanical ventilation-induced acute lung injury

2010 ◽  
Vol 8 (1) ◽  
pp. 3 ◽  
Author(s):  
Adrian Doroszko ◽  
Thomas S Hurst ◽  
Dorota Polewicz ◽  
Jolanta Sawicka ◽  
Justyna Fert-Bober ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Tidal Volume ◽  
High Tidal Volume

scholarly journals Mechanical ventilation-induced apoptosis in newborn rat lung is mediated via FasL/Fas pathway

2013 ◽  
Vol 305 (11) ◽  
pp. L795-L804 ◽  
Author(s):  
Andreas A. Kroon ◽  
Veronica DelRiccio ◽  
Irene Tseu ◽  
Brian P. Kavanagh ◽  
Martin Post
Keyword(s):  
Mechanical Ventilation ◽  
Caspase 3 ◽  
Cyclic Stretch ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Rat Lung ◽  
Newborn Rat ◽  
Lung Epithelial ◽  
Induced Apoptosis

Mechanical ventilation induces pulmonary apoptosis and inhibits alveolar development in preterm infants, but the molecular basis for the apoptotic injury is unknown. The objective was to determine the signaling mechanism(s) of ventilation (stretch)-induced apoptosis in newborn rat lung. Seven-day-old rats were ventilated with room air for 24 h using moderate tidal volumes (8.5 ml/kg). Isolated fetal rat lung epithelial and fibroblast cells were subjected to continuous cyclic stretch (5, 10, or 17% elongation) for up to 12 h. Prolonged ventilation significantly increased the number of apoptotic alveolar type II cells (i.e., terminal deoxynucleotidyl transferase dUTP-mediated nick-end labeling and anti-cleaved caspase-3 immunochemistry) and was associated with increased expression of the apoptotic mediator Fas ligand (FasL). Fetal lung epithelial cells, but not fibroblasts, subjected to maximal (i.e., 17%, but not lesser elongation) cyclic stretch exhibited increased apoptosis (i.e., nuclear fragmentation and DNA laddering), which appeared to be mediated via the extrinsic pathway (increased expression of FasL and cleaved caspase-3, -7, and -8). The intrinsic pathway appeared not to be involved [minimal mitochondrial membrane depolarization (JC-1 flow analysis) and no activation of caspase-9]. Universal caspases inhibition and neutralization of FasL abrogated the stretch-induced apoptosis. Prolonged mechanical ventilation induces apoptosis of alveolar type II cells in newborn rats and the mechanism appears to involve activation of the extrinsic death pathway via the FasL/Fas system.

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