Experimental neurogenic pulmonary edema

1981 ◽  
Vol 54 (5) ◽  
pp. 632-636 ◽  
Author(s):  
Jose Garcia-Uria ◽  
Julian T. Hoff ◽  
Sandra Miranda ◽  
Merry Nishimura
Keyword(s):  
Arterial Hypertension ◽  
Pulmonary Edema ◽  
Main Pulmonary Artery ◽  
Neurogenic Pulmonary Edema ◽  
Increased Intracranial Pressure ◽  
Content Type ◽  
Systemic Arterial Hypertension ◽  
Pulmonary Arterial ◽  
Pressure Changes ◽  
Fine Print

✓ Pressure changes in the aorta, left atrium, and main pulmonary artery were measured before, during, and after inducing increased intracranial pressure in cats. By selectively controlling each of the three pressures, it was concluded that pulmonary arterial hypertension is the single most important precursor of experimental neurogenic pulmonary edema. An earlier observation that neurogenic pulmonary edema may develop in the absence of systemic arterial hypertension was confirmed.

Neurogenic pulmonary edema associated with a colloid cyst in the third ventricle

1980 ◽  
Vol 52 (3) ◽  
pp. 395-398 ◽  
Author(s):  
Gideon Findler ◽  
Shamay Cotev
Keyword(s):  
Pulmonary Edema ◽  
Third Ventricle ◽  
Colloid Cyst ◽  
Neurogenic Pulmonary Edema ◽  
Content Type ◽  
Acute Hydrocephalus ◽  
The Third ◽  
Hypothalamic Nuclei ◽  
Fine Print

✓ Neurogenic pulmonary edema (NPE) is usually the result of head trauma. The authors describe the case of a 13-year-old girl, in whom NPE was associated with a colloid cyst of the third ventricle causing acute hydrocephalus. The mechanisms involved in the development of NPE are briefly discussed. The possible role of the colloid cyst in the distortion of the anatomical relationships in the vicinity of the hypothalamic nuclei is considered.

Experimental neurogenic pulmonary edema

1981 ◽  
Vol 54 (5) ◽  
pp. 627-631 ◽  
Author(s):  
Julian T. Hoff ◽  
Merry Nishimura ◽  
Jose Garcia-Uria ◽  
Sandra Miranda
Keyword(s):  
Pulmonary Edema ◽  
Intracranial Hypertension ◽  
Perfusion Pressure ◽  
Systemic Arterial Pressure ◽  
Neurogenic Pulmonary Edema ◽  
Content Type ◽  
Systemic Arterial Hypertension ◽  
Cushing Response ◽  
Intraventricular Infusion ◽  
Sympathetic Discharge

✓ Neurogenic pulmonary edema (NPE) was produced consistently in normal cats by increasing intracranial pressure with an intraventricular infusion of mock cerebrospinal fluid. The usual elevation of systemic arterial pressure (SAP) that follows severe intracranial hypertension (the “Cushing response”) was controlled by blood withdrawal at variable rates to achieve and maintain constant cerebral perfusion pressure (CPP) in three groups of cats of 50, 20, and 0 mm Hg, respectively, for 30 minutes. In this model, NPE occurs in the absence of increased SAP and in the presence of decreasing CPP. These results indicate that systemic arterial hypertension is not an essential stimulus for the development of NPE, and suggest that the lungs are directly affected by the intense sympathetic discharge evoked by severe intracranial hypertension.

Experimental neurogenic pulmonary edema in cats

1978 ◽  
Vol 48 (3) ◽  
pp. 383-389 ◽  
Author(s):  
Julian T. Hoff ◽  
Merry Nishimura
Keyword(s):  
Gas Exchange ◽  
Pulmonary Edema ◽  
Quantitative Measurement ◽  
Neurogenic Pulmonary Edema ◽  
Lung Water ◽  
Microscopic Appearance ◽  
Content Type ◽  
Intraventricular Infusion ◽  
Normal Lungs ◽  
Fine Print

✓ 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. However, under identical conditions, except that ICP was raised to only 100 mm Hg, three of seven animals did not develop hemorrhagic edema of the lungs and the remaining four had spotty hemorrhage. Thirteen control animals with normal ICP had normal lungs. Gravimetric lung water analysis by Pearce's method confirmed gross and microscopic appearance of hemorrhagic pulmonary edema. Extravascular lung water (p < 0.05) and lung blood (p < 0.05) were significantly greater than control values when ICP was raised to or exceeded 150 mm Hg. Despite hemorrhagic edema, pulmonary gas exchange (O2, CO2) remained unaffected. This animal model allows quantitative measurement of neurogenically-mediated hemorrhagic edema of the lungs before gas exchange is impaired. The model may facilitate clarification of the pathogenesis of neurogenic pulmonary edema and, consequently, refine evaluation of therapy.

Delayed nonfatal pulmonary edema following subarachnoid hemorrhage

1979 ◽  
Vol 51 (6) ◽  
pp. 856-859 ◽  
Author(s):  
Anthony Fisher ◽  
Hesham Tawfik Aboul-Nasr
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Pulmonary Edema ◽  
Response To Therapy ◽  
Neurological Deterioration ◽  
Neurogenic Pulmonary Edema ◽  
Content Type ◽  
Fine Print

✓ A case of neurogenic pulmonary edema (NPE) is reported which is unusual in that it was delayed 4 days after the initial subarachnoid hemorrhage, and occurred at a time when the patient was improving clinically. After a favorable response to therapy, it recurred 48 hours later, again without neurological deterioration. The possible mechanisms in the production of NPE are discussed.

Intracranial xanthogranuloma of the dura in Hand-Schüller-Christian disease

1993 ◽  
Vol 78 (2) ◽  
pp. 297-300 ◽  
Author(s):  
Zain Alabedeen B. Jamjoom ◽  
Vinita Raina ◽  
Abdulfattah Al-Jamali ◽  
Abdulhakim B. Jamjoom ◽  
Basim Yacub ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Clinical Features ◽  
Obstructive Hydrocephalus ◽  
Relevant Literature ◽  
Increased Intracranial Pressure ◽  
Falx Cerebri ◽  
Content Type ◽  
Tentorium Cerebelli ◽  
Ultrastructural Studies ◽  
Fine Print

✓ The authors describe a 37-year-old man with the classic clinical features of Hand-Schüller-Christian disease. He presented with symptoms of increased intracranial pressure due to obstructive hydrocephalus secondary to a huge xanthogranuloma involving falx cerebri and tentorium cerebelli. Immunohistochemical and ultrastructural studies failed to demonstrate Langerhans histiocytes, however. The implication of this finding is discussed in light of the recent relevant literature.

Medulla oblongata edema associated with neurogenic pulmonary edema

1986 ◽  
Vol 64 (3) ◽  
pp. 494-500 ◽  
Author(s):  
Robert H. Brown ◽  
Brian D. Beyerl ◽  
Richard Iseke ◽  
Michael H. Lavyne
Keyword(s):  
Pulmonary Edema ◽  
Brain Stem ◽  
Central Nervous System Disease ◽  
Neurogenic Pulmonary Edema ◽  
Anatomical Location ◽  
Content Type ◽  
Von Hippel Lindau ◽  
System Disease ◽  
Brain Stem Lesions ◽  
Stem Lesions

✓ Neurogenic pulmonary edema (NPE) occurs in association with central nervous system disease without underlying cardiopulmonary problems. It is characterized by profound pulmonary vascular congestion and a fulminant clinical course. Although several reports document a role for experimental brain-stem lesions in the production of NPE, there have been only two studies in man correlating specific brain-stem lesions with NPE. The authors report a case of NPE occurring in a patient with von Hippel-Lindau disease and a dorsal medullary syrinx with postoperative dorsal medullary edema. The anatomical location of this patient's lesion is reviewed in the context of alternative theories of the pathogenesis of NPE.

scholarly journals Early onset of retrograde flow in the main pulmonary artery is a characteristic of pulmonary arterial hypertension

2011 ◽  
Vol 33 (6) ◽  
pp. 1362-1368 ◽  
Author(s):  
Frank Helderman ◽  
Gert-Jan Mauritz ◽  
Kirsten E. Andringa ◽  
Anton Vonk-Noordegraaf ◽  
J. Tim Marcus
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Early Onset ◽  
Main Pulmonary Artery ◽  
Retrograde Flow ◽  
Pulmonary Arterial

Experimental approach for monitoring surface brain pressure

1971 ◽  
Vol 34 (1) ◽  
pp. 38-47 ◽  
Author(s):  
Alfonso Schettini ◽  
Lachlan McKay ◽  
Raymond Majors ◽  
Joseph Mahig ◽  
Arnold H. Nevis
Keyword(s):  
Cerebrospinal Fluid ◽  
Temperature Compensation ◽  
Experimental Approach ◽  
Sensing Element ◽  
Increased Intracranial Pressure ◽  
Content Type ◽  
Brain Surface ◽  
Before And After ◽  
Brain Pressure ◽  
Fine Print

✓ A method for monitoring brain surface pressure through the intact dura has been designed based upon the concept of a coplanar, non-sensitive ring transducer. The transducer detects the underlying brain pressure while the stretching forces of the dural membrane are dissipated at the outer ring. The strain gauge consists of a piezo-resistive silicon-chip sensing element and a dummy element that provides temperature compensation. Cisternal cerebrospinal fluid (CSF) and brain surface pressures were monitored simultaneously in dogs under general anesthesia, both before and after increased intracranial pressure was produced experimentally. A difference was found between CSF and brain surface pressures. Possible explanations for this observation are discussed.

Conray ventriculography in the diagnosis of intraventricular and posterior fossa lesions

1971 ◽  
Vol 34 (3) ◽  
pp. 405-407 ◽  
Author(s):  
Salvador Gonzalez-Cornejo
Keyword(s):  
Intracranial Pressure ◽  
Posterior Fossa ◽  
Increased Intracranial Pressure ◽  
Content Type ◽  
Conray Ventriculography ◽  
Fine Print

✓ The author reports the safe and satisfactory use of Conray ventriculography in 26 patients with increased intracranial pressure and discusses his technique for this procedure.

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