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.

Acute intracranial hypertension and brain-stem blood flow

1984 ◽  
Vol 60 (3) ◽  
pp. 566-571 ◽  
Author(s):  
Seigo Nagao ◽  
Norio Sunami ◽  
Takumi Tsutsui ◽  
Yutaka Honma ◽  
Fumiyuki Momma ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intracranial Hypertension ◽  
Brain Stem ◽  
Inferior Colliculus ◽  
Medulla Oblongata ◽  
Systemic Arterial Pressure ◽  
Content Type ◽  
Cushing Response ◽  
The Mean ◽  
Mass Lesions

✓ This study has been carried out to evaluate the effect of supratentorial mass lesions on the local cerebral blood flow (CBF) of the brain stem. Local CBF of the thalamus, inferior colliculus, and medulla oblongata, and supra- and infratentorial pressure were serially measured in 52 cats with intracranial hypertension produced by supratentorial balloon expansion. The mean control local CBF's in the thalamus, inferior colliculus, and medulla oblongata were 37.5, 42.1, and 30.7 ml/100 gm/min, respectively. At 20 to 30 mm Hg of supratentorial pressure, the local CBF of the thalamus started to decrease, and at 20 mm Hg of infratentorial pressure, the local CBF of the inferior colliculus began to decrease. Finally, at 40 to 60 mm Hg of infratentorial pressure, the local CBF of the medulla oblongata was affected. At the beginning of uncal herniation, indicated by anisocoria, the mean local CBF of the inferior colliculus abruptly decreased from 33.7 to 19.6 ml/100 gm/min in 16 cats. The Cushing response was evoked at a mean supratentorial pressure of 93.4 mm Hg and infratentorial pressure of 49.9 mm Hg in 16 cats. When the systemic arterial pressure was increased to the highest level in 13 cats, the mean local CBF of the medulla oblongata did not show significant change (a decrease from 22.8 to 20.9 ml/100 gm/min). The results suggest that at the beginning of uncal herniation, the local CBF of the upper brain stem markedly decreased. During the Cushing response, the local CBF of the medulla oblongata did not change significantly.

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.

Catecholamine response to a gradual increase of intracranial pressure

1993 ◽  
Vol 79 (5) ◽  
pp. 705-709 ◽  
Author(s):  
Johan van Loon ◽  
Bharati Shivalkar ◽  
Chris Plets ◽  
Jan Goffin ◽  
T. Budya Tjandra-Maga ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Perfusion Pressure ◽  
Gradual Increase ◽  
Hemodynamic Changes ◽  
Content Type ◽  
Catecholamine Response ◽  
Cushing Response ◽  
The Mean ◽  
The Brain

✓ To determine the catecholamine response to progressive intracranial hypertension, intracranial pressure (ICP) was raised gradually by continuous expansion of an epidural balloon in seven dogs. Hemodynamic parameters, ICP, and cerebral perfusion pressure (CPP) were monitored continuously and serum catecholamine levels began to rise when CPP was in the low-positive range (20 to 30 mm Hg), reaching a peak just after brain death (CPP ≤ 0 mm Hg). There was no correlation between ICP and the catecholamine peak. Compared to control values, the mean increase was 286-fold for epinephrine and 78-fold for norepinephrine. Temporally, the catecholamine peak corresponded well with the observed hemodynamic changes. These results suggest that ischemia in certain parts of the brain stem is responsible for the hemodynamic changes observed in intracranial hypertension (such as the Cushing response), and they show that catecholamines play an important role in these hemodynamic changes.

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.

Effect on the Cushing response of different rates of expansion of a supratentorial mass

1978 ◽  
Vol 49 (1) ◽  
pp. 61-70 ◽  
Author(s):  
Abdul Hamid Zidan ◽  
John P. Girvin
Keyword(s):  
Heart Rate ◽  
Full Range ◽  
Blood Gases ◽  
Systemic Arterial Pressure ◽  
Critical Volume ◽  
Experimental Conditions ◽  
Content Type ◽  
Cerebral Dysfunction ◽  
Cushing Response ◽  
Supratentorial Mass

✓ The effects on the three components (respiration, blood pressure, and heart rate) of the Cushing response (CR) were studied in cats by the continuous expansion of a supratentorial balloon. The rate of expansion was varied over the range of 0.006 to 0.6 ml/min, during which systemic arterial pressure, heart rate, respiratory rate, and blood gases were monitored. For the different rates the time the CR took to develop, and the balloon volume required for that development were measured. The final volume (“critical volume”) for eliciting the CR was more or less constant over the full range of rates of infusion (balloon expansion), a fact that supports the Monro-Kellie doctrine. This constancy of critical volume (CCV) gives rise to a highly statistically significant relationship between the rate of infusion and the latency to the production of the CR, and it is described by a power curve. Thus the development of cerebral dysfunction under these experimental conditions is independent of the rate of expansion and only dependent upon this critical volume. Exceptions to this concept of a critical volume, at the extreme of rates of expansion of lesions in patients, are predicted.

Intracranial hypertension and cerebral perfusion pressure: influence on neurological deterioration and outcome in severe head injury

2000 ◽  
Vol 92 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Niels Juul ◽  
Gabrielle F. Morris ◽  
Sharon B. Marshall ◽  
_ _ ◽  
Lawrence F. Marshall
Keyword(s):  
Head Injury ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Severe Head Injury ◽  
Perfusion Pressure ◽  
Neurological Deterioration ◽  
Double Blind ◽  
Content Type ◽  
Fine Print

Object. Recently, a renewed emphasis has been placed on managing severe head injury by elevating cerebral perfusion pressure (CPP), which is defined as the mean arterial pressure minus the intracranial pressure (ICP). Some authors have suggested that CPP is more important in influencing outcome than is intracranial hypertension, a hypothesis that this study was designed to investigate.Methods. The authors examined the relative contribution of these two parameters to outcome in a series of 427 patients prospectively studied in an international, multicenter, randomized, double-blind trial of the N-methyl-d-aspartate antagonist Selfotel. Mortality rates rose from 9.6% in 292 patients who had no clinically defined episodes of neurological deterioration to 56.4% in 117 patients who suffered one or more of these episodes; 18 patients were lost to follow up. Correspondingly, favorable outcome, defined as good or moderate on the Glasgow Outcome Scale at 6 months, fell from 67.8% in patients without neurological deterioration to 29.1% in those with neurological deterioration. In patients who had clinical evidence of neurological deterioration, the relative influence of ICP and CPP on outcome was assessed. The most powerful predictor of neurological worsening was the presence of intracranial hypertension (ICP ≥ 20 mm Hg) either initially or during neurological deterioration. There was no correlation with the CPP as long as the CPP was greater than 60 mm Hg.Conclusions. Treatment protocols for the management of severe head injury should emphasize the immediate reduction of raised ICP to less than 20 mm Hg if possible. A CPP greater than 60 mm Hg appears to have little influence on the outcome of patients with severe head injury.

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.

Experimental cerebral oligemia and ischemia produced by intracranial hypertension

1975 ◽  
Vol 43 (3) ◽  
pp. 308-317 ◽  
Author(s):  
Lawrence F. Marshall ◽  
Felix Durity ◽  
Robert Lounsbury ◽  
David I. Graham ◽  
Frank Welsh ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Neurological Function ◽  
Content Type ◽  
No Reflow ◽  
No Reflow Phenomenon ◽  
Complete Cerebral Ischemia ◽  
Fine Print

✓ Cerebral blood flow, electrical activity, and neurological function were studied in rabbits subjected to either 15 minutes of oligemia (20 torr cerebral perfusion pressure) or complete cerebral ischemia produced by cisterna magna infusion. During oligemia, flow was reduced from 68.4 ± 4.2 ml/100 gm/min to 26.3 ± 4.4 (p < .01), and during ischemia animals had no proven flow. By 5 minutes after oligemia or ischemia significant symmetrical hyperemia occurred and there was no evidence of the no-reflow phenomenon. The electroencephalogram became isoelectric significantly later and returned significantly sooner in oligemia than in ischemia. Oligemic animals had earlier and better return of neurological function than their ischemic counterparts, although postinsult hypocapnia improved functional recovery in both groups. These experiments do not support the concept that oligemia is a more severe insult than complete ischemia. In intracranial hypertension produced by this model, the no-reflow phenomenon does not occur.

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.

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