Experimental neurogenic pulmonary edema

Garcia-Uria, Jose; Hoff, Julian T.; Miranda, Sandra Marina Ribeiro de; Nishimura, Merry

doi:10.3171/jns.1981.54.5.0632

Cited by 23 publications

(6 citation statements)

References 39 publications

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“…Similar results were reported by Garcia-Uria et al (8). This leads us to conclude that, in this feline model, NPE results from causes other than hemodynamic changes.…”

supporting

confidence: 92%

“…velop in cats in the absence of obvious pulmonary hypertension (8,9). The l 1-1 3% increase in lung water from NPE reported here is of magnitude comparable to that reported in other studies ( 15) using the Pearce method (12) for determining EVLW/BFDW.…”

supporting

confidence: 87%

“…Rippe et al ( 17) found similar values using different techniques. The increases in LAP in the present study as well as others (8) were small and thus not likely to be the cause of the edema. LAP peak pressures in group 3 briefly rose to as high as 5 mm Hg.…”

supporting

confidence: 54%

“…Species variations may account for different results from studies with dogs and rats in which hemodynamic influences appear to dominate in the edemagenic response to increased ICP (6,7); in sheep, microvascular recruitment has been established as the cause of increased protein-rich lymph production during raised ICP (1 1); in cats, NPE may develop in the absence of pulmonary hemodynamic influences (3,8,15) as supported by the present findings. A recent study by Marin (1 8) showed that intracisternal injection of veratrine in dogs produced NPE due to both hemodynamic and increased permeability mechanisms.…”

mentioning

confidence: 51%

“…It was concluded that pulmonary hypertension was the cause of the NPE. However, Garcia-Uria et al (8) and Millen and Glauser (9) showed that pulmonary hypertension is not always a prerequisite for the resultant edema in cats. NPE developing from a pulse of pressure applied to the crania of cats were found to be inversely related to pulmonary arterial pressures (3).…”

mentioning

confidence: 99%

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Neurogenic Pulmonary Edema in a Pulmonary Normotensive Model

Beckman¹,

Ginty²,

Gaither³

1987

Experimental Biology and Medicine

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In the present study our aim was to determine whether or not neurogenic pulmonary edema would develop from a brief pulse of intracranial pressure (ICP) in the absence of any obvious pulmonary hypertension. There were three groups of cats: sham-operated controls, ICP only, and ICP plus variable occlusion of the pulmonary artery. Partial occlusion of the pulmonary artery was carried out by placing a ligature around the pulmonary trunk and mechanically constricting the artery to maintain pulmonary arterial pressure (PAP) and left atrial pressure (LAP) at pre-ICP levels. In sham-operated animals the extravascular lung water/blood free dry weight ratio (EVLW/BFDW) was 3.26 k 0.07 and broncho-alveolar lavage (BAL) protein, 6.49 2 0.62 mg/g lung. ICP-only caused a rise in PAP, left atrial pressure, and EVLW/BFDW to 3.67 t-0.08 (P < 0.05). ICP with partial occlusion of the pulmonary artery prevented any rise in PAP or LAP while EVLW/BFDW rose to 3.67 +_ 0.10 (P < 0.05) and BAL protein was 8.37 f 1.27 mg/g lung. Our results show that EVLW/BFDW can increase with neurogenic pulmonary edema in cats in the absence of an obvious increase in pulmonary arterial or left atrial pressure. o 1987 Society for Experimental Biology and Medicine.

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“…Similar results were reported by Garcia-Uria et al (8). This leads us to conclude that, in this feline model, NPE results from causes other than hemodynamic changes.…”

supporting

confidence: 92%

supporting

confidence: 87%

supporting

confidence: 54%

mentioning

confidence: 51%

mentioning

confidence: 99%

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Neurogenic Pulmonary Edema in a Pulmonary Normotensive Model

Beckman¹,

Ginty²,

Gaither³

1987

Experimental Biology and Medicine

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Pulmonary lymphatic flow alterations during intracranial hypertension in sheep

Simon

Bayne

1984

Annals of Neurology

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The role of intracranial hypertension in the genesis of neurogenic pulmonary edema was studied in 25 sheep; cardiopulmonary hemodynamics (aortic, pulmonary arterial, and left atrial pressures and cardiac output) and fluid and protein movement across the pulmonary capillary bed (efferent pulmonary lymph flow and lymph/plasma protein ratio) were monitored. Only when intracranial pressure was raised to equal the baseline mean systemic pressure (75 to 120 Torr) did we observe the expected Cushing response of increased aortic pressure, or any alteration in pulmonary hemodynamics or fluid movement. When pulmonary changes did occur, they included an increase in pulmonary arterial pressure of between 5 and 15 Torr without any notable rise in left atrial pressure, and a sustained doubling of the pulmonary lymph flow with no dilution of the lymph/plasma protein ratio. In 3 additional animals cerebral ischemia alone produced an elevation in systemic pressure (74 Torr over baseline) without change in pulmonary arterial pressure, left atrial pressure, or pulmonary lymph flow. Thus, intracranial hypertension and ischemia both affect systemic pressure, but only the elevated intracranial pressure is followed by changes in the pulmonary circuit. We suggest that these changes in pulmonary vascular pressure, independent of changes in left atrial pressure, produce increased pulmonary transcapillary fluid flux that may result in neurogenic pulmonary edema.

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Ventilatory Support for Pulmonary Failure of the Head Trauma Patient

Hemmer¹

1985

Update in Intensive Care and Emergency Medicine

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Experimental neurogenic pulmonary edema

Cited by 23 publications

References 39 publications

Neurogenic Pulmonary Edema in a Pulmonary Normotensive Model

Neurogenic Pulmonary Edema in a Pulmonary Normotensive Model

Pulmonary lymphatic flow alterations during intracranial hypertension in sheep

Ventilatory Support for Pulmonary Failure of the Head Trauma Patient

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