scholarly journals Mechanisms of neurogenic pulmonary edema development

2008 ◽  
pp. 499-506
Author(s):  
J Šedý ◽  
J Zicha ◽  
J Kuneš ◽  
P Jendelová ◽  
E Syková
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Intracranial Pressure ◽  
Pulmonary Edema ◽  
Current Knowledge ◽  
Experimental Models ◽  
Neurogenic Pulmonary Edema ◽  
Life Threatening ◽  
Life Threatening Complication ◽  
Sympathetic Discharge

Neurogenic pulmonary edema is a life-threatening complication, known for almost 100 years, but its etiopathogenesis is still not completely understood. This review summarizes current knowledge about the etiology and pathophysiology of neurogenic pulmonary edema. The roles of systemic sympathetic discharge, central nervous system trigger zones, intracranial pressure, inflammation and anesthesia in the etiopathogenesis of neurogenic pulmonary edema are considered in detail. The management of the patient and experimental models of neurogenic pulmonary edema are also discussed.

Elevated intracranial pressure increases pulmonary vascular permeability to protein

1989 ◽  
Vol 67 (3) ◽  
pp. 1185-1191 ◽  
Author(s):  
M. D. McClellan ◽  
I. M. Dauber ◽  
J. V. Weil
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Intracranial Pressure ◽  
Pulmonary Edema ◽  
Vascular Permeability ◽  
Elevated Intracranial Pressure ◽  
Hemodynamic Changes ◽  
Pulmonary Vascular Permeability ◽  
Pulmonary Arterial ◽  
Protein Permeability

The syndrome of neurogenic pulmonary edema raises the question of whether there are neurological influences on pulmonary vascular permeability. Previous experimental models commonly produced severe hemodynamic alterations, complicating the distinction of increased permeability from increased hydrostatic forces in the formation of the pulmonary edema. Accordingly, we employed a milder central nervous system insult and measured the pulmonary vascular protein extravasation rate, which is a sensitive and specific indicator of altered protein permeability. After elevating intracranial pressure via cisternal saline infusion in anesthetized dogs, we used a dual isotope method to measure the protein leak index. This elevated intracranial pressure resulted in a nearly three-fold rise in the protein leak index (54.1 +/- 7.5 vs. 20.2 +/- 0.9). This central nervous system insult was associated with only mild increases in pulmonary arterial pressures and cardiac output. However, when we reproduced these hemodynamic changes with left atrial balloon inflation or isoproterenol infusion, we observed no effect on the protein leak index compared with control. Although the pulmonary arterial wedge pressure with intracranial pressure remained <10 mmHg, increases in the extravascular lung water were demonstrated. The results suggest the existence of neurological influences on pulmonary vascular protein permeability. We conclude that neurological insults result in increase pulmonary vascular permeability to protein and subsequent edema formation, which could not be accounted for by hemodynamic changes alone.

Role of central nervous system nitric oxide in the development of neurogenic pulmonary edema in rats

2001 ◽  
Vol 29 (6) ◽  
pp. 1222-1228 ◽  
Author(s):  
Ossama Hamdy ◽  
Hiroshi Maekawa ◽  
Yasuhiro Shimada ◽  
Guo Gang Feng ◽  
Naohisa Ishikawa
Keyword(s):  
Nitric Oxide ◽  
Central Nervous System ◽  
Nervous System ◽  
Pulmonary Edema ◽  
Neurogenic Pulmonary Edema

scholarly journals Neurogenic Pulmonary Edema

2018 ◽  
Vol 21 (1) ◽  
pp. 49-52
Author(s):  
Carlos Eduardo Romeu De Almeida ◽  
Eberval Gadelha Figueiredo ◽  
Bernardo Assumpção De Monaco ◽  
Arthur Maynart Pereira Oliveira ◽  
Manoel Jacobsen Teixeira
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Subarachnoid Hemorrhage ◽  
Lung Injury ◽  
Pulmonary Edema ◽  
Patient Management ◽  
Acute Onset ◽  
Neurogenic Pulmonary Edema ◽  
Alveolar Space ◽  
Pulmonary Vasoconstriction

Neurogenic Pulmonary Edema (NPE) is defined as the acute onset of dyspnea or a decrease in PaO2/FiO2 ratio, following an acute central nervous system (CNS) insult, in the absence of other obvious causes of lung injury. The most important cause of NPE is subarachnoid hemorrhage (SAH), followed by cerebraltrauma and epilepsy. The incidence of NPE after SAH in the literature may vary from 4 to 23% in greater studies, with SAH accounting for 43-73% of cases of NPE. It is postulated that an excessive adrenergic discharge would lead to pulmonary vasoconstriction and a rapid increase in pulmonary capillaryhydrostatic pressure, thus promoting fluid leakage to the alveolar space. NPE is generally treated in a supportive and conservative fashion, and patient management should be focused in the primary insult.

scholarly journals Recurrent Acute Neurogenic Pulmonary Edema after Uncontrolled Seizures

2018 ◽  
Vol 2018 ◽  
pp. 1-4 ◽  
Author(s):  
Daniel C. Sacher ◽  
Erika J. Yoo
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Pulmonary Edema ◽  
Protective Ventilation ◽  
Lung Protective Ventilation ◽  
Neurogenic Pulmonary Edema ◽  
Cardiac Pathology ◽  
Source Of Infection ◽  
The Central Nervous System ◽  
Significant Injury

Acute pulmonary edema following significant injury to the central nervous system is known as neurogenic pulmonary edema (NPE). Commonly seen after significant neurological trauma, NPE has also been described after seizure. While many pathogenic theories have been proposed, the exact mechanism remains unclear. We present a 31-year-old man who developed recurrent acute NPE on two consecutive admissions after experiencing witnessed generalized tonic-clonic (GTC) seizures. Chest radiographs obtained after seizure during both admissions showed bilateral infiltrates which rapidly resolved within 24 hours. He required intubation on each occasion, was placed on lung protective ventilation, and was successfully extubated within 72 hours. There was no identified source of infection, and no cardiac pathology was thought to be contributory.

Neuronal Generation from Somatic Stem Cells: Current Knowledge and Perspectives on the Treatment of Acquired and Degenerative Central Nervous System Disorders

2003 ◽  
Vol 3 (3) ◽  
pp. 247-272 ◽  
Author(s):  
S. Corti ◽  
F. Locatelli ◽  
S. Strazzer ◽  
M. Guglieri ◽  
G. Comi
Keyword(s):  
Stem Cells ◽  
Central Nervous System ◽  
Nervous System ◽  
Current Knowledge ◽  
Somatic Stem Cells ◽  
Central Nervous System Disorders

scholarly journals Correction to: Pulmonary edema following central nervous system lesions induced by a non-mouse-adapted EV71 strain in neonatal BALB/c mice

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Yuefei Jin ◽  
Chao Zhang ◽  
Rongguang Zhang ◽  
Jingchao Ren ◽  
Shuaiyin Chen ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Pulmonary Edema ◽  
Ev71 Strain

An amendment to this paper has been published and can be accessed via the original article.

scholarly journals Plant Species of Sub-Family Valerianaceae—A Review on Its Effect on the Central Nervous System

Plants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 846
Author(s):  
Gitishree Das ◽  
Han-Seung Shin ◽  
Rosa Tundis ◽  
Sandra Gonçalves ◽  
Ourlad Alzeus G. Tantengco ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Plant Species ◽  
Current Knowledge ◽  
Biological Properties ◽  
In Vivo Studies ◽  
Food Species ◽  
The Central Nervous System ◽  
Preclinical And Clinical Studies

Valerianaceae, the sub-family of Caprifoliaceae, contains more than 300 species of annual and perennial herbs, worldwide distributed. Several species are used for their biological properties while some are used as food. Species from the genus Valeriana have been used for their antispasmodic, relaxing, and sedative properties, which have been mainly attributed to the presence of valepotriates, borneol derivatives, and isovalerenic acid. Among this genus, the most common and employed species is Valerianaofficinalis. Although valerian has been traditionally used as a mild sedative, research results are still controversial regarding the role of the different active compounds, the herbal preparations, and the dosage used. The present review is designed to summarize and critically describe the current knowledge on the different plant species belonging to Valerianaceae, their phytochemicals, their uses in the treatment of different diseases with particular emphasis on the effects on the central nervous system. The available information on this sub-family was collected from scientific databases up until year 2020. The following electronic databases were used: PubMed, Scopus, Sci Finder, Web of Science, Science Direct, NCBI, and Google Scholar. The search terms used for this review included Valerianaceae, Valeriana, Centranthus, Fedia, Patrinia, Nardostachys, Plectritis, and Valerianella, phytochemical composition, in vivo studies, Central Nervous System, neuroprotective, antidepressant, antinociceptive, anxiolytic, anxiety, preclinical and clinical studies.

scholarly journals Biology of the repair of central nervous system demyelinated lesions: an appraisal

1996 ◽  
Vol 54 (2) ◽  
pp. 331-334 ◽  
Author(s):  
L. A. V Peireira ◽  
M. A. Cruz-Höfling ◽  
M. S. J. Dertkigil ◽  
D. L. Graça
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Schwann Cells ◽  
Demyelinating Disease ◽  
Experimental Models ◽  
Primitive Cell ◽  
Marked Influence ◽  
Myelin Sheaths ◽  
Human Material ◽  
The Central Nervous System

The integrity of myelin sheaths is maintained by oligodendrocytes and Schwann cells respectively in the central nervous system (CNS) and in the peripheral nervous system. The process of demyelination consisting of the withdrawal of myelin sheaths from their axons is a characteristic feature of multiple sclerosis, the most common human demyelinating disease. Many experimental models have been designed to study the biology of demyelination and remyelination (repair of the lost myelin) in the CNS, due to the difficulties in studying human material. In the ethidium bromide (an intercalating gliotoxic drug) model of demyelination, CNS remyelination may be carried out by surviving oligodendrocytes and/or by cells differentiated from the primitive cell lines or either by Schwann cells that invade the CNS. However, some factors such as the age of the experimental animals, intensity and time of exposure to the intercalating chemical and the topography of the lesions have marked influence on the repair of the tissue.

Descriptive epidemiology and risk factors of primary central nervous system tumors: Current knowledge

2016 ◽  
Vol 172 (1) ◽  
pp. 46-55 ◽  
Author(s):  
C. Pouchieu ◽  
I. Baldi ◽  
A. Gruber ◽  
E. Berteaud ◽  
C. Carles ◽  
...  
Keyword(s):  
Risk Factors ◽  
Central Nervous System ◽  
Nervous System ◽  
Current Knowledge ◽  
Central Nervous System Tumors ◽  
Descriptive Epidemiology ◽  
Nervous System Tumors
Sign in / Sign up

Export Citation Format

Share Document