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Review Article
- Neurosurgery
- Brain-lung interaction: a vicious cycle in traumatic brain injury
- Ariana Alejandra Chacón-Aponte, Érika Andrea Durán-Vargas, Jaime Adolfo Arévalo-Carrillo, Iván David Lozada-Martínez, Maria Paz Bolaño-Romero, Luis Rafael Moscote-Salazar, Pedro Grille, Tariq Janjua
- Acute Crit Care. 2022;37(1):35-44. Published online February 11, 2022
- DOI: https://doi.org/10.4266/acc.2021.01193
- 13,911 View
- 852 Download
- 12 Web of Science
- 15 Crossref
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Abstract
PDF - The brain-lung interaction can seriously affect patients with traumatic brain injury, triggering a vicious cycle that worsens patient prognosis. Although the mechanisms of the interaction are not fully elucidated, several hypotheses, notably the “blast injury” theory or “double hit” model, have been proposed and constitute the basis of its development and progression. The brain and lungs strongly interact via complex pathways from the brain to the lungs but also from the lungs to the brain. The main pulmonary disorders that occur after brain injuries are neurogenic pulmonary edema, acute respiratory distress syndrome, and ventilator-associated pneumonia, and the principal brain disorders after lung injuries include brain hypoxia and intracranial hypertension. All of these conditions are key considerations for management therapies after traumatic brain injury and need exceptional case-by-case monitoring to avoid neurological or pulmonary complications. This review aims to describe the history, pathophysiology, risk factors, characteristics, and complications of brain-lung and lung-brain interactions and the impact of different old and recent modalities of treatment in the context of traumatic brain injury.
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Citations
Citations to this article as recorded by
- Acute brain injury increases pulmonary capillary permeability via sympathetic activation-mediated high fluid shear stress and destruction of the endothelial glycocalyx layer
Na Zhao, Chao Liu, Xinxin Tian, Juan Yang, Tianen Wang
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Wei-Hung Chan, Shih-Ming Huang, Yi-Lin Chiu
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Thao L. Nguyen, Dennis W. Simon, Yi-Chen Lai
Seminars in Pediatric Neurology.2024; : 101120. CrossRef - Ventilatory targets following brain injury
Shaurya Taran, Sarah Wahlster, Chiara Robba
Current Opinion in Critical Care.2023; 29(2): 41. CrossRef - Uncertainty in Neurocritical Care: Recognizing Its Relevance for Clinical Decision Making
Luis Rafael Moscote-Salazar, William A. Florez-Perdomo, Tariq Janjua
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Jia Nong, Patrick M. Glassman, Jacob W. Myerson, Viviana Zuluaga-Ramirez, Alba Rodriguez-Garcia, Alvin Mukalel, Serena Omo-Lamai, Landis R. Walsh, Marco E. Zamora, Xijing Gong, Zhicheng Wang, Kartik Bhamidipati, Raisa Y. Kiseleva, Carlos H. Villa, Colin F
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Jason A. Fawley, Christopher J. Tignanelli, Nicole L. Werner, George Kasotakis, Samuel P. Mandell, Nina E. Glass, David J. Dries, Todd W. Costantini, Lena M. Napolitano
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Mabrouk Bahloul, Karama Bouchaala, Najeh Baccouche, Kamilia Chtara, Hedi Chelly, Mounir Bouaziz
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Hye Ju Yeo
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- Acute brain injury increases pulmonary capillary permeability via sympathetic activation-mediated high fluid shear stress and destruction of the endothelial glycocalyx layer
Original Article
- Collagen Synthesis in an in Vivo Rat Model of Ventilator-induced Lung Injury
- Won Il Choi
- Korean J Crit Care Med. 2006;21(2):109-115.
- 1,317 View
- 14 Download
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Abstract
PDF
- BACKGROUND
Experimentally, maintaining high pressure or high volume ventilation in animal models produces an acute lung injury, however, there was little information on remodeling. We investigated the collagen synthesis in a rat model of ventilator-induced lung injury.
METHODS
Rats were ventilated with room air at 85 breaths/minute for 2 hours either tidal volume 7 ml/kg or 20 ml/kg (V(T)7 or V(T)20, respectively). After 2 hours of ventilation, rats were placed in the chamber for 24 hours. Lung collagen was evaluated by immunohistochemistry (n=5) and collagen was quantitated by collagen assay (n=5). Static compliance (Csta) of the whole lung as obtained from the pressure volume curves.
RESULTS
Type I collagen was an increase in expression in the interstitium with large V(T) (20 ml/ kg) ventilation after 2 hours of mechanical ventilation (MV), and further increased expression after 24 hours of recovery period. Static lung compliance was significantly (p<0.05) decreased in the V(T)20 compared with V(T)7 (0.221+/-0.05 vs 0.305+/-0.06 ml/cm H2O) after 2 hours of MV. There was a further decrease in lung compliance after 24 hours of recovery period (0.144+/-0.07 vs 0.221+/-0.05, p<0.05) in the V(T)20.
CONCLUSIONS
Large tidal volume ventilation causes an increase in type 1 collagen expression with reduction of lung compliance.
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