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Biomedical subjects

E D Robin

Publications and source records attributed to E D Robin.

At least 127 records · Page 7Linked to original sources

Pathogenesis of neurogenic pulmonary oedema.

Evidence suggests that the initial phase of neurogenic pulmonary oedema results from a centrally mediated, massive, sympathetic discharge. It is postulated that this produces intense, generlised, but transient, vasoconstriction with a resultant shift of blood from the high-resistance systemic circulation to the low-resistance pulmonary circulation. Pronounced increases in pulmonary vascular pressures and blood-volume then produce pulmonary oedema because of the hydrostatic effect of increased pulmonary capillary pressure. In addition, pulmonary hypertension and hypervolaemia injure pulmonary blood-vessels, altering pulmonary capillary permeability and producing lung haemorrhage. After the transient systemic and pulmonary vascular hypertension subside, the patient is left with abnormal pulmonary capillary permeability, so that pulmonary oedema persists in the face of normal haemodynamic and cardiac function.

Blood Pressure↗

Total eosinophil counts in the management of bronchial asthma.

Total eosinophil counts were investigated in asthmatic patients to determine their usefulness in the diagnosis and management of steroid-dependent asthma. Counts averaged 122 plus or minus 74 (S.D.) per mm-3 (65 untreated normal subjects) and 43 plus or minus 22 per mm-3 (six prednisone-treated normal subjects). Fifty-two patients with active bronchial asthma showed significant eosinophilia (greater than 350/mm-3 off and greater than 85/mm-3 on steroids), suggesting that eosinophilia is an important diagnostic feature of bronchial asthma. In 14 patients (60 observations), the counts showed significant inverse correlation with specific airway conductance--r equals 0.74, p less than 0.001--and with a variety of other measurements of bronchial dynamics and lung volumes, suggesting that the total eosinophil count reflects asthmatic activity and is useful for regulating steroid dosage and for early detection of exacerbations.

Adrenal Cortex Hormones↗

Transalveolar transport of large polar solutes (sucrose, inulin, and dextran).

The in vivo transalveolar transport of three large polar solutes, sucrose, inulin, and dextran (mol wt 60,000-90,00), was compared with the transport of urea in saline-filled dog lung. Apparent permeability coefficents (p', in cm X sec-1 X 10(6)) were as follows; urea: 2.4 +/- 0.28 (SD) greater than sucrose: 0.64 +/- 0.31 (P less than 0.001) greater than inulin: 0.12 +/- .05 (P less than 0.001)--not different from dextran (mol wt 60,000-90,000): 0.08 +/- .02 (P greater then .01). Calculation of the resistance of the alveolar epithelium compared to total barrier resistance for the various solutes indicates that approximately 90% of the total resistance resides in the alveolar epithelium. Comparison of the ratio of permeability coefficients to the ratio of free-diffusion coefficients in water shows similar values for the three large polar solutes, suggesting that permeation through the alveolar epithelium occurs by means of water-filled channels. The values for permeability coefficients of alveolar epithelium fit into the spectrum of values reported for other epithelial structures (including gall bladder, frog skin, and toad bladder); it seems to have a system of channels with a small number of wide "pores" (greater than 80 A) that permit permeation of large polar solutes and is not a relatively homogeneous structure.

Animals↗

Adaptations of energy metabolism in the cultivated macrophage.

Adaptive changes in energy metabolism, as reflected by pyruvate kinase and cytochrome oxidase activities, were examined during in vitro differentiation of the cultivated macrophage. Serum concentrations of tissue culture media, which directly influence endocytic activity, and ambient oxygen tension were both shown to influence pyruvate kinase and cytochrome oxidase activities. Cells maintained in high serum concentrations (30% newborn calf serum [NBCS]) exhibited a 300-400% increase in pyruvate kinase activity and a 40% increase in cytochrome oxidase activity, whereas cells maintained in low serum concentrations (2% NBCS) exhibited a lesser increase (65%) in pyruvate kinase activity and no change in cytochrome oxidase activity. Anaerobiosis resulted in additional alterations in pyruvate kinase and cytochrome oxidase activities. Cells maintained for 48-72 h under anaerobic conditions exhibited a 500-600% increase in pyruvate kinase activity and a 40% decrease in cytochrome oxidase activity. Increased pyruvate kinase activity was dependent on continued protein synthesis. Enzyme increases occurred in anaerobically cultured cells despite an overall reduction in cell protein synthesis. It is suggested that adaptive changes in pyruvate kinase and cytochrome oxidase activity resulting from alterations in either serum concentration or ambient oxygen tension are regulated by two independent mechanisms. One mechanism is aimed at providing energy for endocytic activity and the other in compensating for impaired oxidative metabolism during anaerobiosis.

Aerobiosis↗

Pulmonary edema. 2.

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Acid-Base Equilibrium↗

Pulmonary edema. 1.

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Biological Transport↗

Implantation of exogenous enzymatic activity in isolated alveolar macrophages.

Alveolar macrophages acquired the capacity to oxidize uric acid after exposure to uricase. Presumably this resulted from intracellular incorporation of the enzyme by endocytosis. This approach may provide a general method for (i) testing regulatory biochemical mechanisms, (ii) therapeutic replacement of deficient regulatory macromolecules, and (iii) studying environmental factors that produce genetic alterations.

Animals↗