Pulmonary vascular transport in sheep

Blake, Lynn H.; Staub, Norman C.

doi:10.1016/0026-2862(76)90018-2

Cited by 48 publications

(14 citation statements)

References 29 publications

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“…8 I do not mean to imply that such a phenomenon never occurs. Indeed, it probably occurs when there is increased hydrostatic pressure in microvessels with injured intercellular junctions as in permeability edemas.…”

Section: Chemicalsmentioning

confidence: 99%

“…8 It is possible to separate, at least partially, protein flow from water flow. The models contain pores of different sizes, some of which are so small that only water and electrolytes can pass through them.…”

mentioning

confidence: 99%

“…The others recovered to their baseline condition within 24-72 hours. 10 When we used our multiple equivalent pore model 8 to explain the animals' condition during the steady state period of maximum increased microvascular permeability, we discovered that only modest loosening of the intercellular junctions was required. In fact, the predicted changes in small and intermediate pore sizes would be difficult to detect even by quantitative electron microscopy.…”

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confidence: 99%

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Pulmonary edema due to increased microvascular permeability to fluid and protein.

Staub¹

1978

Circulation Research

175

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THE USUAL clinical designation of pulmonary edema as either cardiogenic or noncardiogenic implies a pathophysiology that is not necessarily true and, in the case of noncardiogenic edema, is singularly uninformative. A better classification would be one based upon the two major variables in the equation for transvascular fluid flow (Starling's equation), namely, Net fluid flow = conductance x driving pressure or, in symbols,where Qf is the net transvascular fluid flow, K is the fluid filtration coefficient, P is the hydrostatic pressure in the microvascular* lumen (mv) and perimicrovascular* interstitial fluid (pmv), respectively; a is a weighted plasma protein reflection coefficient which determines the "effective" transvascular protein osmotic pressure difference; and II is the protein osmotic pressure in the plasma (mv) and perimicrovascular (pmv) compartments, respectively.According to Equation 1, the two major types of edema are that due to increased driving pressure (high pressure edema) and that due to altered integrity of the microvascular membrane (permeability edema).High pressure edema may be of cardiac origin (increased microvascular hydrostatic pressure due to left atrial hypertension), but it also may occur when cardiac function is normal as in overexpansion of extracellular volume by crystalloid fluid infusions' (increased pulmo-

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Section: Chemicalsmentioning

confidence: 99%

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Pulmonary edema due to increased microvascular permeability to fluid and protein.

Staub¹

1978

Circulation Research

175

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“…However, this is extremely unlikely, because we have shown elsewhere that large rises in microvascular pressure in the lung apparently do not cause any changes in pore configuration. 24 Besides, we detected no changes in lymph protein composition.…”

Section: Physiological Role Of Positive Airway Pressure In Lung Fluidmentioning

confidence: 68%

“…Because of the spatial distribution of lung mass, 24 about 80% of the lung is in zone III (see example in Table 4 of reference 19). Under these conditions, increases in pulmonary vascular distending pressures may not cause further lung stiffening.…”

Section: Discussionmentioning

confidence: 99%

Effect of positive pressure breathing on lung lymph flow and water content in sheep.

Woolverton¹,

Brigham²,

Staub³

1978

Circulation Research

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SUMMARY We studied the effect of 10 cm H 2 O of continuous positive airway pressure breathing (CPAPB) on steady state lung fluid balance. In 9 of 20 chronically instrumented, unanesthetized sheep, we measured lung lymph flow, pulmonary vascular pressure, cardiac output, pleura! pressure, and lymph and plasma protein concentration during a 2-hour baseline period and 3-4 hours of CPAPB. In eight sheep, we measured the same variables after increasing average left atrial pressure by 18 cm H,O to cause mild interstitial edema. At the end of the final experiment, we anesthetized the sheep, removed the lungs, and measured their water content. During CPAPB, pleural and left atrial pressures increased by 5 cm H,O, whereas puhnonary artery pressure increased by 7-10 cm H 2 O. Lung lymph flow as well as lymph and plasma protein concentrations did not change significantly. In six sheep, postmortem lung water content was increased above that predicted but was within the predicted range for the group as a whole. We conclude that moderate CPAPB does not measurably affect the steady state lung fluid balance. More important, however, the rise in puhnonary vascular pressure must have been balanced by a rise in perimicrovascular interstitial fluid pressure since filtration did not change. It appears that the fraction of increased alveolar pressure transmitted to the microvessels was via the perimicrovascular fluid rather than through solid tissue contact.THE IMPROVED arterial blood oxygenation obtained by increasing airway pressure in patients or experimental animals with pulmonary edema is attributed to two mechanisms. The first, and well established one, is by reinflation of collapsed or fluid-filled alveoli. found that positive pressure ventilation markedly increased right lymph duct flow, at least transiently, in anesthetized dogs with acute pulmonary edema. Several other workers, however, found that positive pressure breathing does not reduce lung water content or the rate of fluid accumulation under edemogenic conditions."*" 16 Bo and associates 17 have demonstrated that, at constant vascular pressures, in isolated, perfused rabbit lungs increased alveolar pressure and lung volume sometimes increase fluid filtration. They have analyzed the separate effects of the increased alveolar pressure and the increased lung volume.The importance of having unequivocal data on the effects of positive alveolar pressure in lung fluid balance is important, not only for establishing the rationale for this clinical maneuver, but also because it may aid in establishing the role of interstitial hydrostatic forces which are not directly accessible for measurement. -Kcr(nmv -ripmv), where K is the endothelial fluid conductance, a is the protein reflection coefficient, P is the hydrostatic pressure, and FI is the protein osmotic pressure in the microvascular (mv) and perimicrovascular (pmv) fluids, respectively.We used unanesthetized sheep with chronic lung lymph fistulas 22 to determine the effect of continuous positive pressure airway breathing ...

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Pulmonary Interstitial Spaces and Lymphatics

Taylor

Parker

1985

Comprehensive Physiology

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Pulmonary vascular transport in sheep

Cited by 48 publications

References 29 publications

Pulmonary edema due to increased microvascular permeability to fluid and protein.

Pulmonary edema due to increased microvascular permeability to fluid and protein.

Effect of positive pressure breathing on lung lymph flow and water content in sheep.

Pulmonary Interstitial Spaces and Lymphatics

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