Experimental pulmonary cedema of nervous origin

Cameron, G. R.; De, S. N.

doi:10.1002/path.1700610309

Cited by 89 publications

(31 citation statements)

References 7 publications

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“…Other investigators have found a similar elevation of systemic blood pressure and pulmonary venous pressure after elevating intracranial pressure with bags, balloons (5, 6, 10, 11), and mineral oil (12). Similar hemodynamic changes can be produced by the intracisternal injection of veratrine (13,14), kaolin (15), a thrombin-fibrinogen mixture (16)(17)(18), and the injection of aconitine in the preoptic areas (19). The mechanisms that have been suggested for these hemodynamic changes accompanying elevated intracranial pressure or intracisternal injections include: ischemia (1,20), release of a pressor material (21), venocontriction (22,23), a myocardial intoropic response (22), and somatic and splanchnic shunting (24).…”

Section: Discussionmentioning

confidence: 52%

Hemodynamic effects of elevated cerebrospinal fluid pressure: alterations with adrenergic blockade

Brashear¹,

Ross²

1970

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 52%

Hemodynamic effects of elevated cerebrospinal fluid pressure: alterations with adrenergic blockade

Brashear¹,

Ross²

1970

J. Clin. Invest.

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“…Another way in which acute pulmonary oedema has been produced in rats and rabbits by Cameron and De (1949) and in dogs by Sarnoff and Berglund (1952) was by the intracisternal injection of thrombin and fibrinogen. This appears to be a non-specific irritative action as veratrine intracisternally in rabbits, has the same effect (Jarisch et a!., Horst et al, 1950).…”

Section: Table II Analysis Of Five Cases Of Fatal Pulmonary Embolismmentioning

confidence: 99%

The disturbance of circulation in traumatic paraplegia in acute and late stages: A pathological study

Wolman

1965

Spinal Cord

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“…Previous work in the 20 th century slowly moved away from the early misconception that the so-called hyaline membranes were the result of aspiration of amniotic fluid contents (Blystad, et al, 1951;Cameron and De, 1949;Dick and Pund, 1949;Farber, 1937;Hadders and Dirken, 1955;Johnson, 1923;Johnson and Meyer, 1925;Latham, et al, 1955;Potter, 1950;Potter, 1952;Potter, 1961;Potter and Craig, 1975;Shanklin, 1959;Shanklin, 1976). Firstly, they are mostly protein but do not actually fulfill the definition of hyalin such as that seen in amyloid degeneration (Taylor, 1988) and the term hyaline membrane disease is a simplification of an earlier designation as hyaline-like membranes (Latham, et al, 1955).…”

Section: Discussionmentioning

confidence: 99%

On the pulmonary toxicity of oxygen. 5. Electronic structure and the paramagnetic property of oxygen

Shanklin

2012

Experimental and Molecular Pathology

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Oxygen uptake by the pulmonary circulation is a chemical reaction. The physicochemical attributes of oxygen are critical when studying pulmonary oxygen toxicity. Extent of lung injury depends on the percentage of oxygen in an oxygen:nitrogen mix in polybaric circumstances . Further change in extent of lesion follows when other gases are used in the inhalant mix instead of nitrogen (Shanklin and Lester, 1972), with oxygen at 21-100% of the mix. Comparative subatmospheric oxygen levels down to 3% in hydrogen, helium, nitrogen, argon, or sulfur hexafluoride, were run with and without ventilatory distress by the Farber (1937) model, bilateral cervical vagotomy (BCV). This yielded coherent results indicating a need to consider molecular characteristics at the atomic level. Molecular mass and size, gas viscosity, and thermal conductivity yielded no obvious correlates to lung injury. Saturation of the outer electron shells of the diluents fit the empiric data, prospectively an interaction between oxygen and nitrogen from their electronegativity and closely approximate molecular mass, size, and shape. The lesion is essentially eliminated at 7% oxygen in nitrogen. At 3% oxygen, the least lesion is found with N 2 , H 2 , and SF 6 , all gases with incomplete outer electron shells, allowing for transient, possibly polarized, covalent bonding with oxygen as the significant minority component in the mix. Argon and helium do not interfere with oxygen. With 3% oxygen in argon without BCV, the experiments ran so long (>70 hours) they were terminated once the point had been made. 3% oxygen in argon after BCV yielded a mean survival more than twice that of BCV in air, indicating a remarkable degree of nitrogen interference with oxygen in the respiratory medium of terrestrial animal life. Argon displayed other advantages for the lung compared to nitrogen. Hydrogen, nitrogen, and oxygen are diatomic molecules, a feature which does relate to the extent of lung injury, but only oxygen is paramagnetic.Magnetic effects on lesion formation were tested: [1] with ventilatory distress induced in newborn rabbits, and [2] in young adult female white mice exposed to 100% oxygen without added mechanical distress. A noninvasive model for ventilatory distress, thoracic restraint (TR), with longer mean survivals of 40-50 hours, was employed rather than the Farber model. Parallel runs with TR, one subset receiving 100% oxygen in a plastic chamber resting on six strong ring magnets with measured fields up to +1200 gauss, the other plain 100% oxygen, were performed. Both subsets developed moderate metabolic acidosis with average weight losses circa 25%, but over different time courses, 82.89 ± 4.91 hours in magnetized oxygen, 55.4 per cent longer than the 53.34 ± 9.82 hours in plain oxygen ( p <0.001). The longer survival in magnetized oxygen meant extensive lung injury (99.57 ± 0.42% pleural surface, versus 83.86 ± 14.03%), but the rate of lesion formation was 30.89 per cent faster in plain oxygen (1.5722% per hour) than in magnetized oxygen...

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Experimental pulmonary cedema of nervous origin

Cited by 89 publications

References 7 publications

Hemodynamic effects of elevated cerebrospinal fluid pressure: alterations with adrenergic blockade

Hemodynamic effects of elevated cerebrospinal fluid pressure: alterations with adrenergic blockade

The disturbance of circulation in traumatic paraplegia in acute and late stages: A pathological study

On the pulmonary toxicity of oxygen. 5. Electronic structure and the paramagnetic property of oxygen

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