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N C Staub

Publications and source records attributed to N C Staub.

At least 145 records · Page 8Linked to original sources
PubMed1976

Protein composition of lung fluids in acute alloxan edema in dogs.

In 11 anesthetized dogs with acute alloxan-induced pulmonary edema, we measured the protein composition of 1-mul samples of plasma, free interstitial fluid, alveolar fluid, and airway fluid. We obtained plasma and airway fluid at regular intervals as edema developed. We sampled alveolar fluid by pleural micropuncture in the unfrozen, excised lung and free interstitial fluid from perivascular cuffs in the frozen, excised lung. The average (+/- 1 SD) total protein concentration of plasma was 4.9 +/- 0.6, airway fluid 4.4 +/- 0.7, free interstitial fluid 4.9 +/- 0.7, and alveolar fluid 5.2 +/- 0.8 g/100 ml. The average fractions of albumin were 0.42 +/- 0.05, 0.50 +/- 0.05, 0.49 +/- 0.06, and 0.49 +/- 0.07, respectively. By paired analysis, the protein concentration of interstitial fluid was not significantly different from alveolar fluid. The protein concentration of airway fluid was significantly less than that in interstitial and alveolar fluid. The albumin fraction of the three lung fluids was identical but significantly different from plasma. We conclude that in alloxan-induced pulmonary edema the lung fluids contain high concentrations of protein and the alveolar epithelial membrane becomes freely permeable to protein molecules.

Albumins↗
PubMed1976

Lung lymph and free interstitial fluid protein composition in sheep with edema.

In 10 anesthetized sheep with mild or moderate pulmonary edema we determined whether the protein composition of lung lymph is representative of free interstitial fluid. We measured protein concentration and albumin fraction in 1-mul samples of plasma, lung lymph, and free interstitial fluid. We also measured lung lymph flow. In five sheep with edema caused by increased pulmonary microvascular pressure, the average (+/- 1 SE) plasma protein concentration was 6.0 +/- 0.4 g/100 ml, lung lymph 3.4 +/- 0.2, and interstitial fluid 3.1 +/- 0.3. Lymph flow increased from an average base-line value of 9.4 ml/h to 43.4 ml/h during edema. Average albumin fractions in lymph and interstitial fluid were 0.56 +/- 0.02 and 0.50 +/- 0.01, respectively, compared with 0.44 +/- 0.01 for plasma. In five sheep with increased-permeability edema, average plasma protein concentration was 5.7 +/- 0.3 g/100 ml, lung lymph 4.1 +/- 0.4, and interstitial fluid 4.6 +/- 0.4. Base-line lymph flow was 11.0 ml/h and increased to 27.8 ml/h during edema. Average albumin fractions in lymph and interstitial fluid were 0.53 +/- 0.01 and 0.50 +/- 0.02, respectively, compared with 0.43 +/- 0.01 for plasma. We conclude in both high-pressure and altered-permeability edema, the protein composition of lung lymph collected from the major lung efferent lymphatic is representative of the free interstitial edema fluid.

Albumins↗
PubMed1976

Protein composition of lung fluids in anesthetized dogs with acute cardiogenic edema.

We measured the protein composition of plasma and lung fluids from nine dogs with cardiogenic edema. To produce the edema, we increased left atrial pressure an average of 36 cmH2O by inflating a balloon catheter in the left atrium, infusing norepinephrine, and infusing large volumes of saline or saline-diluted blood. Blood samples were collected every 15 min, and airway fluid was collected from five dogs that developed severe edema. Terminally, the chest was opened and the lungs were removed. Samples of alveolar fluid were taken from the excised lung by direct pleural puncture with micropipettes. The lungs were frozen in liquid nitrogen and samples of free interstitial fluid were taken from the perivascular and peribronchial cuffs. Plasma and lung fluids were analyzed for total protein by the Lowry method and for albumin-globulin fractions by cellulose acetate electrophoresis. The average total protein concentrations (g/100 ml) were--plasma, 2.65; free interstitial fluid, 1.05; alveolar fluid, 1.23; and airway fluid, 1.29. The average albumin fraction of plasma was 0.40; of alveolar fluid, 0.43; and of airway fluid, 0.43. The protein concentrations in the three lung fluids were nearly identical to each other, but were less than half that of plasma. We conclude that in high-pressure pulmonary edema with alveolar flooding, the capillary endothelium retains the ability to restrict protein relative to fluid filtration, but the alveolar epithelium becomes freely permeable to protein.

Acute Disease↗
PubMed1976

Changes in the fluid compartments and dry weights of reimplanted dog lungs.

We studied changes in fluid compartments and dry weights of reimplanted lungs of dogs during the first 6 wk after operation. Excision and reimplantation caused a large increase in lung weight. The increase in weight was maximal 3 days after operation, was proportionately greater in the upper middle lobe than in the lower lobe, and was principally due to increased extravascular water. Dry weight and noncirculating red cells (measured by subtracting 51Cr-labeled red cell mass from total red cell mass as measured by hemoglobin extraction) also increased within 3 days after operation. Lung weight and extravascular water decreased progressively after 3 days and were normal in 6 wk. Chromated blood mass remaining within excised, passively drained lobes did not change at any stage postoperatively. Three days after operation, frozen lung sections showed minimal alveolar fluid but large amounts of peribronchial and perivascular edema which was occasionally blood tinged; submucosal edema was present in a few bronchi. Using intraalveolar Evans blue dye, we confirmed that several bronchial lymphatics close within 6 h and refenerate during the first postoperative week. Many of observed functional changes in freshly reimplanted lungs are temporally related to changes in extravascular water.

Animals↗
PubMed1976

Indicator dilution lung water and capillary blood volume in prolonged heavy exercise in normal men.

The indicator dilution quantity of extravascular water in the lung (idQwl) increases in exercise, but whether it is a real accumulation of fluid or is due to increased distribution of blood flow to previously unperfused regions of alveolar walls is unsettled. In 9 well-trained young men, we compared idQwl and the pulmonary capillary blood volume, as measured by the carbon monoxide diffusing capacity procedure, at rest and after 10 and about 50 min of heavy work (150 watts) on a bicycle ergometer. From rest to 10-min exercise, we observed the following changes. Heart rate 72 +/- 15 beats per min (mean +/- SD) to 151 +/- 23; cardiac output 6.0 +/- 1 liter per min to 17.7 +/- 4.1; carbon monoxide diffusing capacity, 46 +/- 10 ml per min per Hg to 65 "/- 11. These all remained constant between 10- and 50-min exercise. The idQwl increased from 178 +/- 37 ml at rest to 219 +/- 46 ml at 10 min and 233 +/- 43 ml at 50 min, and pulmonary capillary blood volume increased from 140 +/- 52 ml at rest to 220 +/- 106 and 206 +/- 98 at 10 and 50 min of exercise, respectively. All of the changes from rest to early exercise were significant (P less than 0.05) by paired t test. There were no significant changes between early and late exercise. We concluded that the early exercise increase in idQwl was due to redistribution of blood flow among and within alveolar walls. The absence of any increase in idQwl between early and late exercise is evidence against accumulation of lung fluid.

Adolescent↗
PubMed1975

Effect of end-expiratory airway pressure on accumulation of extravascular lung water.

The effect of end-expiratory airway pressure on the accumulation of extravascular lung water during lobar venous occlusion for 2 h was studied in closed-chest artifically ventilated dogs. Dogs were divided into two groups by end-expiratory airway pressures of 0 or 10 cmH2O. High-pressure lobar pulmonary edema was produced by lobar venous occlusion, which elevated microvascular hydrostatic pressure. After occlusion of the lobar pulmonary vein, lobar venous pressure (and microvascular hydrostatic pressure) rapidly became identical to pulmonary arterial pressure. We measured extravascular lung water (post mortem) and pulmonary arterial pressure and calculated plasma colloid osmotic pressure to determine the relationship between the accumulation of lung water and the difference between pulmonary microvascular pressure and plasma colloid osmotic pressure (net intravascular filtration pressure). At comparable net intravascular filtration pressures, dogs ventilated at the higher end-expiratory airway pressure accumulated more extravascular lung water. This study indicates that increasing end-expiratory airway pressure from zero to 10 cmH2O increases the accumulation of extravascular lung water when microvascular hydrostatic pressure is raised.

Animals↗
PubMed1975

Distribution volumes of [131I]albumin, [14C]sucrose, and 36Cl in sheep lung.

We measured the steady-state volumes of distribution for radioactive chloride, sucrose, and albumin in the lung of six anesthetized, spen-thorax sheep. We allowed 2 days for [131I]albumin to equilibrate throughout the body, 2 h for the 36Cl, and a 40-min constant infusion for [14C]sucrose before killing the animal. Five minutes before death, we gave [125I]albumin to tag lung plasma volume. We killed the animals by clamping both lung hila; we then removed the lungs and homogenized them. We measured residual red cell and plasma volume, total extravascular lung water, and the extravascular content of the three tracers. The distribution volumes expressed as fractions of blood-free lung weight were: 36Cl equals 0.44, sucrose equals 0.28, and albumin equals 0.07. If the sucrose distribution volume is taken as the best estimate of the lung's extravascular extracellular space, then chloride clearly overestimates the interstitial fluid volume, being either bound or partially intracellular. On the other hand, albumin clearly underestimates the interstitial fluid volume.

Animals↗
PubMed1975

Effect of increased vascular pressure on lung fluid balance in unanesthetized sheep.

In 20 unanesthetized sheep, we measured lung lymph flow and lymph and plasma protein concentrations during steady-state base-line conditions and during steady-state elevations of pulmonary microvascular hydrostatic pressure (range 3 to 23 cm H2O). In every sheep there was a base-line lung lymph flow (average 5.7 +/- 2.5 (SD) ml/hour), demonstrating that net fluid filtration occurred. The base-line lymph-plasma total protein ratio averaged 0.69 +/- 0.05, indicating a high protein osmotic pressure in the interstitial fluid at the filtration site. Lymph flow increased and lymph protein concentration decreased approximately linearly whenever hydrostatic pressure rose. A new steady-state condition was reached in 1-2 hours. The difference in plasma-to-lymph protein osmotic pressure increased by half the hydrostatic pressure increment (50% negative feedback regulation). Extravascular lung water content, measured post-mortem, did not change significantly until microvascular hydrostatic pressure more than doubled, indicating a large safety factor that protects the lungs against fluid accumulation normally. The major contributions to the safety factor appeared to be a sensitive and efficient lymph pump coupled to a washout of interstitial protein. The fluid filtration coefficient, whose calculation required many assumptions, averaged 1.64 +/- 2.65 ml/(cm H2O times hour) in the base-line condition and did not change significantly over the pressure range studied.

Albumins↗
PubMed1975

Effect of acute hemorrhagic shock on pulmonary microvascular fluid filtration and protein permeability in sheep.

In an attempt to further delineate the pathophysiology of the shock-lung syndrome, we studied the effect of hemorrhagic shock on the pulmonary microcirculation in the adult sheep with lung lymph flow and lymph protein transport as indices of fluid filtration and vascular permeability to protein. We noted that lymph flow remained at baseline levels during shock, despite significant decreases in pulmonary artery and left atrial pressures. This suggests that microvascular pressure is maintained by an increase in pulmonary venous resistance. We demonstrated that lymph protein transport does not increase during shock, which indicates that a change in pulmonary vascular permeability to protein does not occur.

Acute Disease↗
PubMed1974

Pulmonary edema.

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Body Fluids↗