Impact of respiratory pattern on lung mechanics and interstitial proteoglycans in spontaneously breathing anaesthetized healthy rats

Moriondo, Andrea; Marcozzi, Cristiana; Bianchin, F.; Passi, Alberto; Boschetti, Federica; Lattanzio, Stefano; Severgnini, Paolo; Pelosi, Paolo; Negrini, Daniela

doi:10.1111/j.1748-1716.2011.02317.x

Cited by 18 publications

(13 citation statements)

References 27 publications

(35 reference statements)

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“…Higher respiratory rate in spontaneously breathing rats led to increased activation of lung tissue metalloproteinases and reduced integrity of the extracellular matrix in the lung [31]. Wang et al reported an association between metalloproteinase 9 and upregulation of iNOS via nuclear factor-κβ [32].…”

Section: Discussionmentioning

confidence: 99%

Lung Protective Ventilation Induces Immunotolerance and Nitric Oxide Metabolites in Porcine Experimental Postoperative Sepsis

et al. 2013

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Low tidal volume ventilation is beneficial in patients with severe pulmonary dysfunction and would, in theory, reduce postoperative complications if implemented during routine surgery. The study aimed to investigate whether low tidal volume ventilation and high positive end-expiratory pressure (PEEP) in a large animal model of postoperative sepsis would attenuate the systemic inflammatory response and organ dysfunction. Thirty healthy pigs were randomized to three groups: Group Prot-7h, i.e. protective ventilation for 7 h, was ventilated with a tidal volume of 6 mL x kg-1 for 7 h; group Prot-5h, i.e. protective ventilation for 5 h, was ventilated with a tidal volume of 10 mL x kg-1 for 2 h, after which the group was ventilated with a tidal volume of 6 mL x kg-1; and a control group that was ventilated with a tidal volume of 10 mL x kg-1 for 7 h. In groups Prot-7h and Prot-5h PEEP was 5 cmH2O for 2 h and 10 cmH2O for 5 h. In the control group PEEP was 5 cmH2O for the entire experiment. After surgery for 2 h, postoperative sepsis was simulated with an endotoxin infusion for 5 h. Low tidal volume ventilation combined with higher PEEP led to lower levels of interleukin 6 and 10 in plasma, higher PaO2/FiO2, better preserved functional residual capacity and lower plasma troponin I as compared with animals ventilated with a medium high tidal volume and lower PEEP. The beneficial effects of protective ventilation were seen despite greater reductions in cardiac index and oxygen delivery index. In the immediate postoperative phase low VT ventilation with higher PEEP was associated with reduced ex vivo plasma capacity to produce TNF-α upon endotoxin stimulation and higher nitrite levels in urine. These findings might represent mechanistic explanations for the attenuation of systemic inflammation and inflammatory-induced organ dysfunction.

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Section: Discussionmentioning

confidence: 99%

Lung Protective Ventilation Induces Immunotolerance and Nitric Oxide Metabolites in Porcine Experimental Postoperative Sepsis

et al. 2013

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“…Also, the duration of the experiment was quite short (3 hours), so that different effects might be observed with longer periods of mechanical ventilation. Lastly, the type of sedation during spontaneous breathing and paralyzing agents during mechanical ventilation may affect lung inflammation [14,15]. …”

mentioning

confidence: 99%

The lung and the brain: a dangerous cross-talk

Pelosi

Rocco

2011

Crit Care

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Brain or lung injury or both are frequent causes of admission to intensive care units and are associated with high morbidity and mortality rates. Mechanical ventilation, which is commonly used in the management of these critically ill patients, can induce an inflammatory response, which may be involved in distal organ failure. Thus, there may be a complex crosstalk between the lungs and other organs, including the brain. Interestingly, survivors from acute lung injury/acute respiratory distress syndrome frequently have some cognitive deterioration at hospital discharge. Such neurologic dysfunction might be a secondary marker of injury and the neuroanatomical substrate for downstream impairment of other organs. Brainlung interactions have received little attention in the literature, but recent evidence suggests that both the lungs and brain can promote inflammation through common mediators. The present commentary discusses the main physiological issues related to brain-lung interactions.

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“…On the other hand, Al Jamal et al showed that extremely high VT (30 ml/kg) and high respiratory rate (90 breaths/minute) induce the expression of versican (CS-PG), basement membrane HS-proteoglycan (HS-PG), and biglycan in lung tissue [16]. Moriondo et al also observed CS and HS fragmentation at high VT [6] and showed that the fluid overload associated with high-VT mechanical ventilation worsened GAG fragmentation, mainly in the ventral lung regions [13].…”

Section: The Ecm and Ventilator-induced Lung Injurymentioning

confidence: 93%

“…Recently, breathing patterns induced by different anesthetic regimens were shown to trigger disorganization and/or remodeling of the ECM. An anesthetic mixture of pentobarbital/urethane led to fragmentation of heparan sulfate (HS) and chondroitin sulfate (CS) [13]. In addition, at low VT, application of positive end-expiratory pressure (PEEP) seems to be protective [14], mainly in the ventral lung regions [15], reducing disruption of GAGs and PGs [14,15].…”

Section: The Ecm and Ventilator-induced Lung Injurymentioning

confidence: 99%

“…MV with physiologi-cal VT induces increased expression and activity of MMP-2 and MMP-9 over time [13], while high VT induces increased expression and release of MMPs by macrophages and epithelial and endothelial cells in response to mechanical stress [6]. Moreover, Foda et al observed that MMPs play an important role in the development of VILI in an in vivo rat model of high-volume ventilation [19].…”

Section: The Ecm and Ventilator-induced Lung Injurymentioning

confidence: 99%

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Role of the extracellular matrix in the genesis of ventilator-induced lung injury

Cruz

Rocco

Pelosi

2017

Med Klin Intensivmed Notfmed

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Impact of respiratory pattern on lung mechanics and interstitial proteoglycans in spontaneously breathing anaesthetized healthy rats

Abstract: This study suggests that the breathing pattern induced by the different anaesthetic regimen may damage the pulmonary interstitium even during spontaneous breathing at physiological tidal volumes.

Cited by 18 publications

References 27 publications

Lung Protective Ventilation Induces Immunotolerance and Nitric Oxide Metabolites in Porcine Experimental Postoperative Sepsis

Lung Protective Ventilation Induces Immunotolerance and Nitric Oxide Metabolites in Porcine Experimental Postoperative Sepsis

The lung and the brain: a dangerous cross-talk

Role of the extracellular matrix in the genesis of ventilator-induced lung injury

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