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.

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.

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.

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.

Accurate reference measurement for postmortem lung water

1984 ◽  
Vol 56 (1) ◽  
pp. 248-253 ◽  
Author(s):  
M. Julien ◽  
M. R. Flick ◽  
J. M. Hoeffel ◽  
J. F. Murray
Keyword(s):  
High Pressure ◽  
Pulmonary Edema ◽  
Extravascular Lung Water ◽  
Blood Cells ◽  
Dry Mass ◽  
Hydroxyproline Content ◽  
Lung Water ◽  
Lung Weight ◽  
Residual Blood ◽  
Normal Lungs

To test the hypothesis that dry blood-free lung weight is increased during pulmonary edema, thereby leading to an underestimation of the ratio of extravascular lung water-to-dry lung weight, we measured postmortem lung water, dry mass, and hydroxyproline content in 33 sheep with normal lungs (n = 10), high-pressure edema (n = 9), or increased permeability edema (n = 14). Residual blood in the lung, measured using hemoglobin as the intravascular marker in all sheep, and also using 51Cr-tagged red blood cells in 24 sheep, was not different between the two methods or among the three groups of sheep. Extravascular lung water increased 64% in sheep with high-pressure edema and 82% in those with increased permeability edema compared with control values. Dry blood-free lung weight was significantly greater (33% more than control values) in sheep with increased permeability edema, causing the ratio of extravascular lung water-to-dry blood-free lung weight to underestimate accumulated lung water by about 50%. Because hydroxyproline content of the lung was not affected by edema, the ratio of extravascular lung water-to-lung hydroxyproline content was more accurate than the ratio of extravascular lung water-to-dry blood-free lung weight in the quantification of pulmonary edema.

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.

A canine model of neurogenic pulmonary edema

1985 ◽  
Vol 59 (3) ◽  
pp. 1019-1025 ◽  
Author(s):  
M. B. Maron
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Edema ◽  
Pulmonary Arterial Pressure ◽  
Canine Model ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Neurogenic Pulmonary Edema ◽  
Lung Water ◽  
Pulmonary Arterial ◽  
Alpha Chloralose

The purpose of this study was to evaluate the usefulness of the intracisternal administration of veratrine as a model of neurogenic pulmonary edema (NPE) in the alpha-chloralose-anesthetized dog. Veratrine (40–60 micrograms/kg) was injected into the cisterna magna of 17 animals, and systemic arterial, pulmonary arterial, and left ventricular end-diastolic (LVEDP) pressures were followed for 1 h. Eleven animals developed alveolar edema. In these animals, systemic arterial pressure increased to 273 +/- 9 (SE) Torr, pulmonary arterial pressure to 74.5 +/- 4.9 Torr, and LVEDP to 42.8 +/- 4.5 Torr, and large amounts of pink frothy fluid, with protein concentrations ranging from 48 to 93% of plasma, appeared in the airways. Postmortem extravascular lung water content (Qwl/dQl) averaged 7.30 +/- 0.46 g H2O/g dry lung wt. Six animals escaped developing this massive degree of edema after veratrine (Qwl/dQl = 4.45 +/- 0.24). These animals exhibited similar elevated systemic arterial pressures (268 +/- 15 Torr), but did not develop the degree of pulmonary hypertension (pulmonary arterial pressure = 52.5 +/- 6.7 Torr, LVEDP = 24.8 +/- 4.0 Torr) observed in the other group. These results suggest that both hemodynamic and permeability mechanisms may play a role in the development of this form of edema and that veratrine administration may provide a useful model of NPE.

Opposing Effects of Isoflurane and Sevoflurane on Neurogenic Pulmonary Edema Development in an Animal Model

2005 ◽  
Vol 102 (6) ◽  
pp. 1182-1189 ◽  
Author(s):  
Nobuhisa Kandatsu ◽  
Yong-Shan Nan ◽  
Guo-Gang Feng ◽  
Kimitoshi Nishiwaki ◽  
Mitsuru Hirokawa ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Animal Model ◽  
Growth Factor ◽  
Pulmonary Edema ◽  
Neurogenic Pulmonary Edema ◽  
Vascular Endothelial ◽  
Lung Water ◽  
Index Of Severity ◽  
Opposing Effects ◽  
Endothelial Growth Factor

Background The current study was undertaken to investigate the effects of pretreatment with isoflurane and sevoflurane on the development of neurogenic pulmonary edema in an animal model. Methods Rats were exposed to room air (control), 1.5% isoflurane, or 2.5% sevoflurane for 4 h. They were then anesthetized with intraperitoneal injections of pentobarbital sodium, and fibrinogen and thrombin were injected into the cisterna magna to induce neurogenic pulmonary edema. Results Consecutive injections of fibrinogen and thrombin caused increases in blood pressure, with the peak values obtained in the isoflurane and sevoflurane groups being lower than the control values. The incidence of significant neurogenic pulmonary edema was 58%, 100%, and 8% in the control, isoflurane, and sevoflurane groups, respectively. The lung water ratio, an index of severity of edema, was 4.86 +/- 0.78, 6.15 +/- 0.64, and 4.40 +/- 0.32 in the control, isoflurane, and sevoflurane groups, respectively. Furthermore, immunohistochemical staining for vascular endothelial growth factor demonstrated an increase of expression in the rat lungs exposed to isoflurane. Treatment with an anti-vascular endothelial growth factor antibody during exposure to isoflurane completely inhibited the effect of isoflurane to promote neurogenic pulmonary edema in this model. Conclusion Exposure to 1.5% isoflurane enhances the development of neurogenic pulmonary edema development in this animal model, most likely via release of vascular endothelial growth factor from bronchial epithelial cells, an effect not observed with sevoflurane.

Primary carcinoma of the pituitary with metastasis to the brain stem

1972 ◽  
Vol 36 (6) ◽  
pp. 781-784 ◽  
Author(s):  
Alan S. Fleischer ◽  
Thomas Reagan ◽  
Joseph Ransohoff
Keyword(s):  
Brain Stem ◽  
Primary Carcinoma ◽  
Microscopic Appearance ◽  
Content Type ◽  
The Brain ◽  
Fine Print

✓ A case of primary carcinoma of the pituitary with metastasis to the brain stem is presented. Although both tumors had the microscopic appearance of benign adenomas, the infiltrative characteristics necessitated the diagnosis of carcinoma.

Histopathology of transistory traumatic paraplegia in the monkey

1971 ◽  
Vol 35 (3) ◽  
pp. 272-276 ◽  
Author(s):  
Franklin C. Wagner ◽  
George J. Dohrmann ◽  
Paul C. Bucy
Keyword(s):  
Spinal Cord ◽  
Gray Matter ◽  
Internal Layers ◽  
Central Gray Matter ◽  
Microscopic Appearance ◽  
Content Type ◽  
Injured Area ◽  
Hemorrhagic Lesion ◽  
Central Gray ◽  
Fine Print

✓ The microscopic appearance of the primate spinal cord within a 4-hour interval following the delivery of a direct force sufficient to produce a transitory paraplegia was investigated by light microscopy. The resulting hemorrhagic lesion involved primarily the central gray matter and was attributed to the direct effect of the trauma on the vessels in the gray matter with a consequent impairment of blood supply to the injured area. Chromatolysis, vacuolation, and alterations in cytoplasmic density and stainability were observed within the neurons. The edematous changes in the white matter, which were more marked in the internal layers relative to the external layers, appeared minimal and explain in part why the paraplegia was transient.

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