Results 151 to 160 of about 650,154 (185)
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Pathogenetic Mechanisms of Neurogenic Pulmonary Edema
Journal of Neurotrauma, 2015Neurogenic pulmonary edema (NPE) is a life-threatening complication of central nervous system (CNS) injuries. This review summarizes current knowledge about NPE etiology and pathophysiology with an emphasis on its experimental models, including our spinal cord compression model.
Josef Zicha, Jaroslav Kunes
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Prevalence, in-hospital mortality, and factors related to neurogenic pulmonary edema after spontaneous subarachnoid hemorrhage: a systematic review and meta-analysis [PDF]
Neurosurgical Review, 2023 Chunling Li, Guo Tang
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DNase-1 Treatment Exerts Protective Effects in Neurogenic Pulmonary Edema via Regulating the Neutrophil Extracellular Traps after Subarachnoid Hemorrhage in Mice [PDF]
Journal of Clinical Medicine, 2022 Hanhai Zeng, Gao Chen
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Clinics in Chest Medicine, 1985
Neurogenic pulmonary edema is an anomaly because it cannot be categorized into either of the two major types of pulmonary edema. Both high-pressure and increased-permeability abnormalities may be involved in the pathogenesis of neurogenic pulmonary edema. Furthermore, the mechanisms responsible for these abnormalities appear quite complex.
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Neurogenic pulmonary edema is an anomaly because it cannot be categorized into either of the two major types of pulmonary edema. Both high-pressure and increased-permeability abnormalities may be involved in the pathogenesis of neurogenic pulmonary edema. Furthermore, the mechanisms responsible for these abnormalities appear quite complex.
openaire +2 more sources
Mechanism of neurogenic pulmonary edema∗
The American Journal of Cardiology, 1967Abstract The mechanism of paroxysmal pulmonary edema following brain injury or irritation is discussed after a review of older and recent experimental studies. It is concluded that both a systolic and a diastolic overload of the left ventricle, connected with sympathetic stimulation, are necessary elements.
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American Journal of Roentgenology, 1971
Patients who sustain head trauma, with or without seizures, or who develop increased pressure for other reasons should be suspect for the development of pulmonary edema. Early recognition may avoid confusion with congestive heart failure. This distinction is of importance since the usual drugs used in the treatment of congestive heart failure are ...
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Patients who sustain head trauma, with or without seizures, or who develop increased pressure for other reasons should be suspect for the development of pulmonary edema. Early recognition may avoid confusion with congestive heart failure. This distinction is of importance since the usual drugs used in the treatment of congestive heart failure are ...
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Chlorpromazine treatment for neurogenic pulmonary edema
Critical Care Medicine, 1985A patient with neurogenic pulmonary edema was successfully treated with the alpha-blocking agent, chlorpromazine. A pathophysiologic basis for this drug's efficacy is discussed.
R N, Wohns +3 more
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Neurogenic Pulmonary Edema and Missile Emboli
The Journal of Trauma: Injury, Infection, and Critical Care, 1980A case of missile emboli to a major intracranial vessel resulting in fulminant pulmonary edema is reported. A discussion of the etiology of neurogenic pulmonary edema (NPE) is presented. The cause is thought to be a marked increase in pulmonary artery pressure, due to a massive catechol release in the CNS, and possibly secondary to post-capillary ...
H D, Reines +3 more
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A Change of Position for Neurogenic Pulmonary Edema
Neurocritical Care, 2008Stroke is the third most common cause of death in the Western World and is a condition seen by Neurologists, General Physicians and Primary Care Physicians. Neurogenic pulmonary edema can complicate the management of large strokes and cerebral hemorrhage.
Scott A, Marshall, Paul, Nyquist
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Experimental neurogenic pulmonary edema in cats
Journal of Neurosurgery, 1978✓ Hemorrhagic pulmonary edema was produced consistently in 19 of 20 anesthetized, paralyzed, ventilated cats when intracranial pressure (ICP) was raised for 30 minutes by intraventricular infusion of mock CSF to 150 mm Hg in 14, or 200 mm Hg in six.
J T, Hoff, M, Nishimura
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