Low Tidal Volume and High Positive End-Expiratory Pressure Mechanical Ventilation Results in Increased Inflammation and Ventilator-Associated Lung Injury in Normal Lungs

2010 ◽  
Vol 110 (6) ◽  
pp. 1652-1660 ◽  
Author(s):  
Caron M. Hong ◽  
Da-Zhong Xu ◽  
Qi Lu ◽  
Yunhui Cheng ◽  
Vadim Pisarenko ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Tidal Volume ◽  
Positive End Expiratory Pressure ◽  
Low Tidal Volume ◽  
Normal Lungs

scholarly journals Inhibition of Poly(Adenosine Diphosphate–Ribose) Polymerase Attenuates Ventilator-induced Lung Injury

2008 ◽  
Vol 108 (2) ◽  
pp. 261-268 ◽  
Author(s):  
Rosanna Vaschetto ◽  
Jan W. Kuiper ◽  
Shyh Ren Chiang ◽  
Jack J. Haitsma ◽  
Jonathan W. Juco ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Tidal Volume ◽  
Interleukin 6 ◽  
Inflammatory Responses ◽  
Adenosine Diphosphate ◽  
High Tidal Volume ◽  
Positive End Expiratory Pressure ◽  
Ventilator Induced Lung Injury ◽  
Pharmacologic Inhibition

Background Mechanical ventilation can induce organ injury associated with overwhelming inflammatory responses. Excessive activation of poly(adenosine diphosphate-ribose) polymerase enzyme after massive DNA damage may aggravate inflammatory responses. Therefore, the authors hypothesized that the pharmacologic inhibition of poly(adenosine diphosphate-ribose) polymerase by PJ-34 would attenuate ventilator-induced lung injury. Methods Anesthetized rats were subjected to intratracheal instillation of lipopolysaccharide at a dose of 6 mg/kg. The animals were then randomly assigned to receive mechanical ventilation at either low tidal volume (6 ml/kg) with 5 cm H2O positive end-expiratory pressure or high tidal volume (15 ml/kg) with zero positive end-expiratory pressure, in the presence and absence of intravenous administration of PJ-34. Results The high-tidal-volume ventilation resulted in an increase in poly(adenosine diphosphate-ribose) polymerase activity in the lung. The treatment with PJ-34 maintained a greater oxygenation and a lower airway plateau pressure than the vehicle control group. This was associated with a decreased level of interleukin 6, active plasminogen activator inhibitor 1 in the lung, attenuated leukocyte lung transmigration, and reduced pulmonary edema and apoptosis. The administration of PJ-34 also decreased the systemic levels of tumor necrosis factor alpha and interleukin 6, and attenuated the degree of apoptosis in the kidney. Conclusion The pharmacologic inhibition of poly(adenosine diphosphate-ribose) polymerase reduces ventilator-induced lung injury and protects kidney function.

scholarly journals Influence of positive end-expiratory pressure (PEEP) on histopathological and bacteriological aspects of pneumonia during low tidal volume mechanical ventilation

2004 ◽  
Vol 30 (12) ◽  
pp. 2263-2270 ◽  
Author(s):  
Pierre Emmanuel Charles ◽  
Laurent Martin ◽  
Manuel Etienne ◽  
Delphine Croisier ◽  
Lionel Piroth ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Tidal Volume ◽  
Positive End Expiratory Pressure ◽  
Low Tidal Volume

Mechanical Ventilation Affects Lung Function and Cytokine Production in an Experimental Model of Endotoxemia

2005 ◽  
Vol 102 (2) ◽  
pp. 331-339 ◽  
Author(s):  
Fabienne Brégeon ◽  
Stéphane Delpierre ◽  
Bruno Chetaille ◽  
Osamu Kajikawa ◽  
Thomas R Martin ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Tidal Volume ◽  
Blood Gases ◽  
Lung Mechanics ◽  
Positive Pressure ◽  
Positive End Expiratory Pressure ◽  
Cell Counts ◽  
Volume Controlled Ventilation ◽  
Spontaneously Breathing

Background Mechanical ventilation using tidal volumes around 10 ml/kg and zero positive end-expiratory pressure is still commonly used in anesthesia. This strategy has been shown to aggravate lung injury and inflammation in preinjured lungs but not in healthy lungs. In this study, the authors investigated whether this strategy would result in lung injury during transient endotoxemia in the lungs of healthy animals. Methods Volume-controlled ventilation with a tidal volume of 10 ml/kg and zero positive end-expiratory pressure was applied in two groups of anesthetized-paralyzed rabbits receiving either intravenous injection of 5 mug/kg Escherichia coli lipopolysaccharide (n = 10) or saline (n = 10) 2 h after the start of mechanical ventilation. The third group consisted of 10 spontaneously breathing anesthetized animals receiving lipopolysaccharide. Anesthesia was then continued for 4 h in the three groups while the ventilatory modes were maintained unchanged. Lung injury was studied using blood gases, respiratory physiologic variables, analysis of the bronchoalveolar lavage cell counts, and cytokine concentrations and lung pathologic examination. Results Significant histologic lung alterations, hypoxemia, and altered lung mechanics were observed in rabbits treated with mechanical ventilation and intravenous lipopolysaccharide but not in the mechanically ventilated animals injected with saline or in spontaneously breathing animals treated with lipopolysaccharide. Endotoxemic ventilated animals also had significantly more lung inflammation as assessed by the alveolar concentration of neutrophils, and the concentrations of the chemokines interleukin 8 and growth-related oncogen alpha. Conclusions These results showed that positive-pressure mechanical ventilation using a tidal volume of 10 ml/kg and zero positive end-expiratory pressure was harmful in the setting of endotoxemia, suggesting that the use of this ventilator strategy in the operating room may predispose to lung injury when endotoxemia occurs.

scholarly journals Open lung approach with low tidal volume mechanical ventilation attenuates lung injury in rats with massive brain damage

Critical Care ◽  
2014 ◽  
Vol 18 (2) ◽  
pp. R59 ◽  
Author(s):  
Joerg Krebs ◽  
Charalambos Tsagogiorgas ◽  
Paolo Pelosi ◽  
Patricia RM Rocco ◽  
Maximilia Hottenrott ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Tidal Volume ◽  
Brain Damage ◽  
Open Lung ◽  
Low Tidal Volume ◽  
Open Lung Approach

scholarly journals Regional Lung Derecruitment and Inflammation during 16 Hours of Mechanical Ventilation in Supine Healthy Sheep

2013 ◽  
Vol 119 (1) ◽  
pp. 156-165 ◽  
Author(s):  
Mauro R. Tucci ◽  
Eduardo L. V. Costa ◽  
Tyler J. Wellman ◽  
Guido Musch ◽  
Tilo Winkler ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Regions Of Interest ◽  
Positive End Expiratory Pressure ◽  
18F Fluorodeoxyglucose ◽  
Positron Emission ◽  
Lung Dysfunction ◽  
Regional Lung ◽  
Net Uptake ◽  
Normal Lungs

Abstract Background: Lung derecruitment is common during general anesthesia. Mechanical ventilation with physiological tidal volumes could magnify derecruitment, and produce lung dysfunction and inflammation. The authors used positron emission tomography to study the process of derecruitment in normal lungs ventilated for 16 h and the corresponding changes in regional lung perfusion and inflammation. Methods: Six anesthetized supine sheep were ventilated with VT = 8 ml/kg and positive end-expiratory pressure = 0. Transmission scans were performed at 2-h intervals to assess regional aeration. Emission scans were acquired at baseline and after 16 h for the following tracers: (1) 18F-fluorodeoxyglucose to evaluate lung inflammation and (2) 13NN to calculate regional perfusion and shunt fraction. Results: Gas fraction decreased from baseline to 16 h in dorsal (0.31 ± 0.13 to 0.14 ± 0.12, P < 0.01), but not in ventral regions (0.61 ± 0.03 to 0.63 ± 0.07, P = nonsignificant), with time constants of 1.5–44.6 h. Although the vertical distribution of relative perfusion did not change from baseline to 16 h, shunt increased in dorsal regions (0.34 ± 0.23 to 0.63 ± 0.35, P < 0.01). The average pulmonary net 18F-fluorodeoxyglucose uptake rate in six regions of interest along the ventral–dorsal direction increased from 3.4 ± 1.4 at baseline to 4.1 ± 1.5⋅10−3/min after 16 h (P < 0.01), and the corresponding average regions of interest 18F-fluorodeoxyglucose phosphorylation rate increased from 2.0 ± 0.2 to 2.5 ± 0.2⋅10−2/min (P < 0.01). Conclusions: When normal lungs are mechanically ventilated without positive end-expiratory pressure, loss of aeration occurs continuously for several hours and is preferentially localized to dorsal regions. Progressive lung derecruitment was associated with increased regional shunt, implying an insufficient hypoxic pulmonary vasoconstriction. The increased pulmonary net uptake and phosphorylation rates of 18F-fluorodeoxyglucose suggest an incipient inflammation in these initially normal lungs.

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