Interaction cerveau-poumon

Abdennour, L.; Zeghal, C.; Dème, M.; Puybasset, L.

doi:10.1016/j.annfar.2012.04.013

Cited by 63Respiratory Support and MechanismsTakotsubo Cardiomyopathy and Associated PhenomenaTraumatic Brain Injury and Neurovascular Disturbances

Interaction cerveau-poumon

Abdennour, L., Zeghal, C., Dème, M., Puybasset, L.·2012·Annales Françaises d Anesthésie et de Réanimation

DOI 10.1016/j.annfar.2012.04.013

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Abstract

The brain and the lungs interact early and rapidly when hit by a disease process. Often well tolerated by the healthy brain, an impaired respiratory function may deteriorate further a "sick" brain. Hypoxemia is a prognostic factor in the brain-injured patients. At the opposite, an acute brain damage early impacts the lung function. Local brain inflammation spreads rapidly to the lung. It initiates an immunological process weakening the lungs and increasing its susceptibility to infection and mechanical ventilation. Sometimes this process is preceded by a swelling lesion, known as neurogenic pulmonary oedema, resulting from an sympathetic overstimulation which usually follows an intense and brutal surge of intracranial pressure. The management of brain-injured patients has to be directed toward the protection of both the brain and lung. Neuronal preservation is crucial, because of the lack of regenerative potential in the brain, unlike the lung. A compromise must be obtained between the cerebral and pulmonary treatments although they may conflict in some situations.

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Lung virus proliferation causes alveolar/interstitial inflammation and edema, leading to CNS hypoxia and increased anaerobic metabolism in brain cells.
“When a virus proliferates in lung tissue cells, it causes diffuse alveolar and interstitial inflammatory exudation, edema, and the formation of transparent membranes. This, in turn, leads to alveolar gas exchange disorders causing hypoxia in the CNS, increasing anaerobic metabolism in the mitochondria of brain cells (Abdennour et al., 2012).”
From Nervous system involvement after infection with COVID-19 and other coronaviruses (2020) · cites this paper as Abdennour et al., 2012

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Authors: Abdennour, L., Zeghal, C., Dème, M., & Puybasset, L.
Affiliations: Pitié-Salpêtrière Hospital (FR)
Corresponding author: Abdennour, L.
ORCID: Abdennour, L.
Puybasset, L.
Venue: Annales Françaises d Anesthésie et de Réanimation
Publisher: Elsevier BV
Published: 2012-06
Volume: 31
Issue: 6
Pages: e101-e107
ISSN: 0750-7658 (ISSN-L)
DOI: 10.1016/j.annfar.2012.04.013
OpenAlex: W170514599
Cited by: 63
References: 34
Citations by year: 2026: 1 · 2025: 2 · 2024: 1 · 2023: 3 · 2022: 13 · 2021: 16 · 2020: 24 · 2016: 1 · 2015: 1
FWCI: 0.05
Type: journal article
Language: fr
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Annales Françaises d Anesthésie et de Réanimation (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Respiratory Support and Mechanisms
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Takotsubo Cardiomyopathy and Associated Phenomena
Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Keywords: brain injury, hypoxemia, neurogenic pulmonary edema, neuroinflammation, systemic inflammatory response, intracranial pressure, mechanical ventilation, lung infection susceptibility, neuroprotection, lung protection, prognostic factors, neurocritical care
MeSH terms: Brain Diseases, Brain Injuries, Hypoxia, Brain, Encephalitis, Humans, Intracranial Pressure, Lung, Lung Diseases, Pulmonary Edema, Respiration, Artificial, Disease Progression, Hyperoxia

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