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

2017 ◽  
Vol 14 (1) ◽  
Author(s):  
Yuefei Jin ◽  
Chao Zhang ◽  
Rongguang Zhang ◽  
Jingchao Ren ◽  
Shuaiyin Chen ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Pulmonary Edema ◽  
Ev71 Strain

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.

Pulmonary Reflexes in Pulmonary Edema?

1957 ◽  
Vol 189 (1) ◽  
pp. 132-136 ◽  
Author(s):  
C. Aravanis ◽  
A. Libretti ◽  
E. Jona ◽  
J. F. Polli ◽  
C. K. Liu ◽  
...  
Keyword(s):  
Central Nervous System ◽  
High Pressure ◽  
Nervous System ◽  
Pulmonary Artery ◽  
Pulmonary Edema ◽  
Pulmonary Veins ◽  
Systemic Circulation ◽  
Left Ventricular ◽  
Additional Element ◽  
Stimulation Of

The mechanism of pulmonary edema caused by stimulation of the central nervous system was studied in 33 dogs. Stimulation was obtained by the intracisternal injection of veratrine, or of air or saline under high pressure, or by electric stimulation of the hypothalamus. Pressure changes in the pulmonary artery, left atrium and left ventricle were recorded by means of three catheters introduced through the right external jugular vein and the left femoral artery. Experiments were performed with closed or open chest, and following ligation of the thoracic aorta and inferior cava. Lung opacity was studied as a means to estimate the blood content of this organ. Data obtained in closed-chest experiments suggest that a blood shift from the systemic to the pulmonary circulation may be a factor in veratrine-induced pulmonary edema. This was confirmed by the observation that, following mechanical exclusion of the systemic circulation, no pulmonary edema occurred while the changes of left ventricular pressure were minimal and inconstant. In these animals, pulmonary artery pressure still rose indicating vasoconstriction while an increase of lung opacity suggested that the vasoconstriction was greater in the pulmonary veins than in the arteries. Injection of air or saline under high pressure into the cisterna magna and faradic stimulation of the hypothalamus caused pulmonary hypertension, even after exclusion of the systemic circulation. In these experiments, a decreased lung opacity suggested that the pulmonary constriction was greater on the arterial than on the venous side. These findings are offered as evidence that the caliber of the pulmonary vessels may be influenced by central nervous system stimulation, an additional element to be considered in the mechanism of pulmonary edema.

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 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.

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.

Development of Tolerance to Ozone in Reference to Pulmonary Edema

1957 ◽  
Vol 190 (1) ◽  
pp. 84-88 ◽  
Author(s):  
Richard N. Matzen
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Pulmonary Edema ◽  
Alveolar Hemorrhage ◽  
Low Concentrations ◽  
Bronchial Inflammation ◽  
The Central Nervous System ◽  
Challenging Dose ◽  
High Concentrations ◽  
Development Of Tolerance

Massive pulmonary edema, varying degrees of alveolar hemorrhage and tracheo-bronchial inflammation occur in animals exposed to high concentrations of ozone. Initial exposures to low concentrations of ozone can prevent the formation of edema and death on subsequent severe exposures in mice. This tolerance was shown to be detectable in 24 hours and present for as long as 102 days. Protection is rendered against a challenging dose as high as 2 1/2 times the ld50. The signs caused by exposure suggest that the central nervous system may be affected as well as the lungs.

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