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Biomedical subjects

N C Staub

Publications and source records attributed to N C Staub.

At least 127 records · Page 7Linked to original sources
PubMed1979

Equilibration of intravascular albumin with lung lymph in unanesthetized sheep.

In 16 unanesthetized sheep with chronic lung lymph fistulas we measured pulmonary vascular pressures, lymph flow, lymph and plasma total protein and albumin concentration. We determined the rate of equilibration of radioiodinated albumin between plasma and lung interstitial fluid (lung lymph) in three steady-state conditions; baseline (n = 14), increased pulmonary microvascular pressure (n = 9) and increased microvascular permeability (n = 4). The tracer protein equilibration proceeded according to single compartment wash-in kinetics in all experiments. Lung lymph flow averaged 5.3 +/- 2.8 (S.D.)ml/h under baseline conditions, 16.1 +/- 10.6 ml/h during increased pressure and 37.3 +/- 29.4 ml/h during increased permeability. The half time of equilibration averaged 2.9 +/- 1.0 h, 2.2 +/- 1.0 h and 0.7 +/- 0.2 h, respectively. Lung interstitial fluid equilibrates with plasma proteins more rapidly than most other organs. The marked difference between increased permeability and the other conditions demonstrates the sensitivity of this method. No evidence was obtained that any tracer protein entered lung lymph within the caudal mediastinal lymph node.

Animals↗
PubMed1978

Pulmonary edema: physiologic approaches to management.

The integrity of the normal endothelial barrier is responsible for two of the three major safety factors preventing pulmonary edema. This is why edema due to increased pressure is usually not as severe as edema due to increased permeability. Management ought to follow sound physiologic principles. These principles are to lower microvascular hydrostatic pressure and to provide adequate supportive therapy. Positive end-expiratory pressure may improve arterial oxygen transport, but there is no evidence that it improves the balance of pulmonary fluid in edema. Raising the microvascular protein osmotic pressure may be beneficial in edema due to increased pressure but has no demonstrated rationale in edema due to increased permeability.

Blood Proteins↗
PubMed1977

Role of bulk fluid flow in protein permeability of the dog lung alveolar membrane.

In five anesthetized, closed-thorax dogs, we measured net tracer albumin (RISA) uptake rate from an isosmotic buffer-filled lung lobe for 6 h; 3 h at each of two different alveolar RISA concentrations. We calculated the permeability coefficient assuming a two-compartment (alveolar fluid and plasma) diffusional model. In every dog the permeability coefficient decreased after the alveolar RISA concentration was increased. After freezing the lungs terminally, we found the fluid-filled lobes had extensive free interstitial fluid perivascular cuffs, indicating a third compartment filled by bulk flow. In separate experiments, we filled isolated lung lobes with buffer containing RISA and microsampled free interstitial fluid. The free interstitial fluid RISA concentration averaged 90% of airway concentration. The interstitium appears to fill by bulk flow through low-resistance channels. Tracer protein uptake from a fluid-filled lung lobe involves three fluid compartments. We postulate fluid and protein enter the interstitium by bulk flow along a hydrostatic pressure gradient, and protein then diffuses into plasma from the interstitium.

Animals↗
PubMed1977

Extravascular lung water after extracellular fluid volume expansion in dogs.

We have compared extravascular lung water after extracellular fluid volume expansion with that predicted from lung sucrose space measured in control dogs. In control lungs mean extravascular water:dry weight ratio was 3.81 +/- 0.16 (SD) (n = 5) and extravascular sucrose space/dry weight was 1.79 +/- 0.45 (n = 4). After acute expansion of extracellular fluid volume by 10% of body weight mean extravascular water:dry lung weight was 4.17 +/- 0.27 (m = 5), less than half the predicted increase to 4.63 +/- 0.19, suggesting some degree of protection. After 20% (n = 4), 30% (n = 2), and 40% (n = 1) expansion, no protection was demonstrated and there was considerable scatter of lung water at each infusion volume. When volume expansion increased pulmonary capillary intravascular forces (due to decreased protein osmotic pressure and increased hydrostatic pressure) by more than 20 cmH2O there was a linear increase in extravascular lung water with increasing intravascular forces. Three dogs did not conform to this relationship and had disproportionately large increases in lung water, possibly due to alveolar flooding.

Animals↗
PubMed1977

Proportions of dog lung lymph in the thoracic and right lymph ducts.

We studied the external lymphatic drainage of the lung in anesthetized dogs, by simultaneously measuring lymph flows from the thoracic duct (TD) and right lymph duct (RLD) during base line and during pulmonary edema. We measured lymph flow for a 2-h base-line period, for 2 h after tying off the thoracic duct above the diaphragm to eliminate nonthoracic lymph contributions, and after giving alloxan. Following alloxan, all dogs developed moderately severe pulmonary edema. In eight dogs the average TD flows were 24.0, 0.9, and 8.2 ml/h and RLD flows were 1.1, 1.3, and 8.4 ml/h, respectively. If we assume that all increases in lymph flow after giving alloxan are due to increased lung lymph flow, then, on the average, 50% of lung lymph drains into the TD and 50% into the RLD. However, among the eight dogs, four had significant increases in TD flow after alloxan (8.9-24.6 ml/h), and four did not. RLD flow increased in all dogs following alloxan. It appears the fraction of lung lymph draining into the TD and RLD can vary greatly amone individual dogs but, on the average, the TD and RLD receive about equal fractions of the pulmonary lymph. In shamoperated control animals TD and RLD lymph flows did not change over a 5-h period.

Alloxan↗
PubMed1977

Effects of alveolar hypoxia on lung fluid and protein transport in unanesthetized sheep.

To determine whether hypoxia directly affects pulmonary microvascular filtration of fluid or permeability to plasma proteins, we measured steady state lung lymph flow and protein transport in eight unanesthetized sheep breathing 10% O2 in N2 for 4 hours. We also studied three sheep breathing the same gas mixture for 48 hours. We surgically prepared the sheep to isolate and collect lung lymph and to measure average pulmonary arterial (Ppa) and left atrial (Pla) pressures. We placed a balloon catheter in the left atrium to elevate Pla. After recovery, the sheep breathed air through a tracheostomy for 2-4 hours, followed by 4 or 48 hours of hypoxia. In 13 4-hour studies, the average arterial PO2 fell from 97 to 38 torr; Ppa rose from 20 to 33 cm H2O; and lung lymph flow and lymph protein flow were unchanged. We also found that during 48-hour hypoxia, with a sustained elevation in Ppa and a decline in Pla, lymph flow and protein flow did not increase. In four sheep, we also raised Pla for 4 hours, followed by 4 hours of hypoxia with elevated Pla. Again, despite the added stress of elevated Pla, we found that lymph flow and lymph protein flow remained constant during hypoxia. We conclude that severe alveolar hypoxia, for 4 or 48 hours, alone or with increased pulmonary microvascular pressure, produced no change in lung fluid filtration or protein permeability, a finding supported by normal postmortem histology and extravascular lung water content.

Acute Disease↗
PubMed1976

Mechanism of alveolar flooding in acute pulmonary oedema.

In severe pulmonary oedema, the alveoli fill rapidly with fluid of essentially the same protein composition as free interstitial fluid. The usual explanation is that the normally 'tight' alveolar epithelial intercellular junctions suddenly become freely permeable to proteins. But the pathophysiological basis for such a change is unknown. In seven anaesthetized dogs one lower lobe was filled with iso-osmotic fluid containing 125I-labelled albumin. The calculated alveolus-blood albumin permeability over three hours averaged 0.06 X 10(-7) cm/s. It decreased nearly 50% when the alveolar tracer concentration was tripled for three more hours. At autopsy, large interstitial free fluid cuffs around blood vessels and airways were found. Isolated lung lobes were filled with isosmotic fluid containing tracer albumin at 10 and 20 cmH2O (0.98-1.96 kPa) airway pressure. Free interstitial fluid cuffs developed within 30 and 10 minutes, respectively. The tracer protein concentration in the cuff fluid averaged 0.9 that of the alveolar fluid. It is postulated that the terminal airway epithelium is normally permeable to protein and water. In acute pulmonary oedema alveolar flooding may occur along the same pathway after the loose interstitial tissue space is fluid-filled and its pressure exceeds that in the airway. The anatomical site of the bulk fluid and protein leak has not been identified.

Acute Disease↗