Pathogenesis of Pulmonary Edema by Alloxan

Aviado, Domingo M.; Schmidt, Carl F.

doi:10.1161/01.res.5.2.180

Cited by 31 publications

(14 citation statements)

References 11 publications

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“…Normalization of the activity of the tracer is thus required. In 1957 Aviado and Schmidt attempted to follow the development of alloxaninduced pulmonary edema using diffusible ( 131 I-albumin) and nondiffusible ( 32 P-labeled red blood cells) tracers [43]. Due to technological limitations, they could only use one tracer in each animal.…”

Section: Imaging Of Pulmonary Microvascular Permeabilitymentioning

confidence: 99%

Real Time Lung Imaging for the Detection of Lung Injury and Alveolar Fluid Movement During Mechanical Ventilation

Prost¹,

Ricard²,

Saumon³

et al. 2010

TONMEDJ

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Experimental ventilator-induced lung injury (VILI) is characterized by alterations in alveolar epithelial and microvascular permeability that favors the systemic dissemination of lung borne cytokines or bacteria. Animal models of VILI have been shown relevant to patient care and outcome and help explaining why most patients with the acute respiratory distress syndrome do not die from respiratory failure but from multiple organ dysfunction. Recent experimental studies also showed that adverse ventilator patterns may propel airway secretions and bacteria to previously healthy lung regions. Noninvasive imaging techniques were used for years to study the net rate of protein flow across the pulmonary microvascular endothelium and the alveolar epithelium in vivo, during normal breathing and lung inflation. More recently, the two-way protein fluxes across the alveolo-capillary barrier and the intra-pulmonary dispersion of alveolar edema have been monitored during mechanical ventilation. These experiments have provided new insights on the mechanisms of experimental VILI that may be of clinical value. This review will describe the evolution of these techniques and their main physiological and pharmacological applications in the era of VILI.

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Section: Imaging Of Pulmonary Microvascular Permeabilitymentioning

confidence: 99%

Real Time Lung Imaging for the Detection of Lung Injury and Alveolar Fluid Movement During Mechanical Ventilation

Prost¹,

Ricard²,

Saumon³

et al. 2010

TONMEDJ

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“…Born (21) and Aviado et al (22) have reported that edematous changes can be produced in the excised lung by perfusing it with a solution containing SH-inhibitors such as alloxan, parachloromercuribenzoate, iodoacetic acid and N-ethylmaleimide. However, administration of these compounds into living animals is not associated with a consistent production of pulmonary edema; because the injurious effect of these compounds is not specific to the lung.…”

Section: Pathology Of the Pulmonary Alterations In Ratsmentioning

confidence: 99%

Experimental Pulmonary Edema in Rodents Following a Single Injection of 4-Nitroquinoline 1-Oxide

Hayashi

Hasegawa

Katayama

1970

Japanese Journal of Pharmacology

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Administration of 4-nitroquinoline 1-oxide has been known to produce pulmonary tumors in rodents (1-3). An electron microscopic examination on the lung of rats shortly after an injection of this compound revealed induction of nucleolar segregation in the alveolar epithelial cells (4). In this experiment, it was further shown that an injection of 4-nitroquinoline 1-oxide could produce pulmonary edema in rats as well as in guinea pigs and rabbits. MATERIALS AND METHODS Pulmonary alterations in ratsMale Sprague-Dawley rats of 4 to 5 week age were used. The test substance, 4 nitroquinoline 1-oxide was suspended in olive oil and subcutaneously injected into rats at interscapular region. The experiments were conducted in two series;Preliminary experiment: Five groups of 10 rats each received an injection of 4-nitro quinoline 1-oxide in dose levels ranging from 10.0 mg/kg to 24.1 mg/kg. During seven days after injection, all rats were checked for general condition, and the rats which died or became moribund were autopsied. Pathological examination of the pulmonary alterations: Thirty-six rats were given an injection of 4-nitroquinoline 1-oxide in a dose of 20 mg/kg, and 6 rats each were sacri ficed 8, 24, 36, 48 and 56 hours after injection. The lungs were excised fresh, weighed and fixed in 10% formalin or Bouin's solution for histology. As the control group , addi tional 8 rats were given a subcutaneous injection of 0.1 ml olive oil, and killed 56 hours after injection. Species difference Male ICR mice of 4 week age, male Hartley guinea-pigs weighing around 300 g and male albino rabbits weighing around 2 kg were given a subcutaneous injection of 4-nitro quinoline 1-oxide in dose levels as shown in Table 2. The animals either died or became moribund were autopsied. The lungs were grossly inspected, weighed and fixed in 10% formalin for histology. The animals which survived for 3 days were decapitated under Nembutal anesthesia, and the lungs were examined in the manner mentioned above.

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“…For this study alloxaninduced pulmonary edema in dogs was chosen because it is the most thoroughly studied (6,7,30). Since alloxan alters vascular pressures very little (6, 7), does not increase capillary blood volume (7), and increases permeability to protein in isolated lungs (29), the edema is apparently a result of loss of vascular integrity.…”

Section: Introductionmentioning

confidence: 99%

In Vivo Assessment of Pulmonary Vascular Integrity in Experimental Pulmonary Edema

Brigham¹,

Snell²

1973

J. Clin. Invest.

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A B S T R A C T During single pass indicator studies across the lungs ["C]urea remains in the vascular compartment, but its molecular size and solubility suggest it might escape abnormally permeable vessels. To test the hypothesis that ["C]urea might be used to distinguish pulmonary edema due to acutely increased intravascular pressure from that due to vascular damage by alloxan, we studied [5tCr]erythrocytes (r), ['I]albumin (a), ["C]urea (u), and tritiated water as dilution indicators in the pulmonary circulation of anesthetized dogs. In addition, the adequacy of albumin as an intravascular indicator was evaluated.Indicator curves, blood gases, hematocrit, and vascular pressures were determined during a base-line period and repeated 30 and 60 min after treatment in five groups of dogs: (a) saline control, (b) alloxan edema, (c) epinephrine infusion, (d) volume overload, and (e) left atrial (LA) balloon obstruction.Groups b, d, and e developed a similar degree of edema judging by wet/dry lung weights and histology. Groups a and c did not develop edema. In alloxan edema, differences between the mean transit time volume of u and r (V.-.) increased over base line at 30 (P < 0.01 ) and 60 min (P < 0.02); the differences between the mean transit time volume of a and r (V.-,) increased slightly at 30 (P < 0.03) and 60 min (P <0.02); and V.-, significantly exceeded V.-, at 30 (mean difference = 9 ml, P < 0.02) and 60 min (mean difference = 11, P < 0.04). In none of the other groups did V.-, significantly exceed V.-,. Thus, comparison of V.-, with V.-, may permit distinction between "high pressure" and "increased permeability" pulmonary edema.Albumin was not a consistently reliable indicator of intravascular volume as compared with composite red cell and albumin curve.

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Pathogenesis of Pulmonary Edema by Alloxan

Cited by 31 publications

References 11 publications

Real Time Lung Imaging for the Detection of Lung Injury and Alveolar Fluid Movement During Mechanical Ventilation

Real Time Lung Imaging for the Detection of Lung Injury and Alveolar Fluid Movement During Mechanical Ventilation

Experimental Pulmonary Edema in Rodents Following a Single Injection of 4-Nitroquinoline 1-Oxide

In Vivo Assessment of Pulmonary Vascular Integrity in Experimental Pulmonary Edema

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