Effect of transpulmonary and vascular pressures on rate of pulmonary edema formation

1977 ◽  
Vol 43 (1) ◽  
pp. 14-19 ◽  
Author(s):  
H. S. Goldberg ◽  
W. Mitzner ◽  
G. Batra
Keyword(s):  
Weight Gain ◽  
Pulmonary Edema ◽  
Transpulmonary Pressure ◽  
Fluid Accumulation ◽  
Edema Formation ◽  
Extravascular Fluid ◽  
Zone Ii ◽  
Vascular Beds

The effect of transpulmonary pressure (Ptp) on rate of extravascular fluid accumulation in isolated canine left lower lobes perfused at constant vascular pressures was investigated. Changes in rate of extravascular fluid accumulation were estimated by changes in rate of slow weight gain. Mean inflow pressure (Ppa) was constant at 34 cmH2O. Mean outflow pressure (Ppv) was constant at either 27.2 cmH2O or 13.6 cmH2O. When increasing Ptp is associated with a derecruitment of vascular beds as the lung changes from predominantly zone III toward zone II, or zone I, there is a decrease in rate of weight gain. When increasing Ptp is not associated with a derecruitment of vascular beds, it is impossible on the basis of these experiments to predict the change in rate of weight gain.

Effect of lung volume history on rate of edema formation in isolated canine lobe

1978 ◽  
Vol 45 (6) ◽  
pp. 880-884 ◽  
Author(s):  
H. S. Goldberg
Keyword(s):  
Weight Gain ◽  
Hydrostatic Pressure ◽  
Lung Volume ◽  
Interstitial Fluid ◽  
Venous Pressure ◽  
Transpulmonary Pressure ◽  
Fluid Accumulation ◽  
Edema Formation ◽  
Lung Inflation ◽  
Volume History

The effect of lung volume history and prior accumulation of interstitial fluid on rate of edema formation in isolated canine lobes was investigated. Mean pulmonary artery pressure and mean pulmonary venous pressure were kept constant at 40 and 30 cmH2O, respectively. Transpulmonary pressure (Ptp) was varied among 5, 15, and 25 cmH2O by progressive stepwise inflation and deflation. Rate of fluid accumulation was estimated by changes in slow weight gain after a change in Ptp. Although there is continuous interstitial fluid accumulation over the course of the experiment the results indicate that interstitial hydrostatic pressure around leaky vessels at Ptp of 15 cmH2O is reduced by prior lung inflation to Ptp of 25 cmH2O and increased by prior deflation to Ptp of 5 cmH2O. These results suggest that the distribution of interstitial fluid may vary as a function of lung volume history.

Evidence for increased intrathoracic fluid volume in man at high altitude

1979 ◽  
Vol 47 (4) ◽  
pp. 670-676 ◽  
Author(s):  
J. J. Jaeger ◽  
J. T. Sylvester ◽  
A. Cymerman ◽  
J. J. Berberich ◽  
J. C. Denniston ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Transpulmonary Pressure ◽  
Fluid Volume ◽  
Pulmonary Mechanics ◽  
Volume Curve ◽  
Extravascular Fluid ◽  
Pressure Volume Curve ◽  
Transthoracic Electrical Impedance ◽  
Extravascular Fluid Volume

To determine if subclinical pulmonary edema occurs commonly at high altitude, 25 soldiers participated in two consecutive 72-h field exercises, the first at low altitude (200–875 m) and the second at high altitude (3,000–4,300 m). Various aspects of ventilatory function and pulmonary mechanics were measured at 0, 36, and 72 h of each exercise. Based on physical examination and chest radiographs there was no evidence of pulmonary edema at high altitude. There was, however, an immediate and sustained decrease in vital capacity and transthoracic electrical impedance as well as a clockwise rotation of the transpulmonary pressure-volume curve. In contrast, closing capacity and residual volume did not change immediately upon arrival at high altitude but did increase later during the exposure. These observations are consistent with an abrupt increase in thoracic intravascular fluid volume upon arrival at high altitude followed by a more gradual increase in extravascular fluid volume in the peribronchial spaces of dependent lung regions.

scholarly journals Effects of Ischemic Acute Kidney Injury on Lung Water Balance: Nephrogenic Pulmonary Edema?

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Rajit K. Basu ◽  
Derek Wheeler
Keyword(s):  
Acute Kidney Injury ◽  
Pulmonary Edema ◽  
Disease Process ◽  
Kidney Injury ◽  
Fluid Accumulation ◽  
Lung Water ◽  
Edema Formation ◽  
Bulk Fluid ◽  
Capillary Membrane ◽  
Alveolar Capillary

Pulmonary edema worsens the morbidity and increases the mortality of critically ill patients. Mechanistically, edema formation in the lung is a result of net flow across the alveolar capillary membrane, dependent on the relationship of hydrostatic and oncotic pressures. Traditionally, the contribution of acute kidney injury (AKI) to the formation of pulmonary edema has been attributed to bulk fluid accumulation, increasing capillary hydrostatic pressure and the gradient favoring net flow into the alveolar spaces. Recent research has revealed more subtle, and distant, effects of AKI. In this review we discuss the concept of nephrogenic pulmonary edema. Pro-inflammatory gene upregulation, chemokine over-expression, altered biochemical channel function, and apoptotic dysregulation manifest in the lung are now understood as “extra-renal” and pulmonary effects of AKI. AKI should be counted as a disease process that alters the endothelial integrity of the alveolar capillary barrier and has the potential to overpower the ability of the lung to regulate fluid balance. Nephrogenic pulmonary edema, therefore, is the net effect of fluid accumulation in the lung as a result of both the macroscopic and microscopic effects of AKI.

Changes in microvascular permeability with acceleration of edema in dog lungs

1990 ◽  
Vol 258 (2) ◽  
pp. H395-H399 ◽  
Author(s):  
B. D. Butler ◽  
R. E. Drake ◽  
W. D. Sneider ◽  
S. J. Allen ◽  
J. C. Gabel
Keyword(s):  
Weight Gain ◽  
Pulmonary Edema ◽  
Membrane Permeability ◽  
Left Atrial ◽  
Membrane Filtration ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Base Line ◽  
Edema Formation ◽  
Before And After

Elevation of left atrial pressure to 25–40 mmHg causes continuous pulmonary edema formation in dog lungs. However, after 5–120 min, the rate of edema formation often increases (acceleration of edema). Acceleration of edema could be associated with an increase in microvascular membrane permeability because an increase in permeability would cause fluid to filter through the microvascular membrane more rapidly. To test the hypothesis that acceleration is associated with increased permeability, we used the continuous weight-gain technique to estimate the pulmonary microvascular membrane filtration coefficient (Kf) before and after acceleration of edema in 10 dogs. Acceleration occurred 36 +/- 38 (SD) min after elevation of left atrial pressure to 35.2 +/- 5.4 mmHg. Rate of weight gain increased from 0.47 +/- 0.17 g/min before acceleration to 0.88 +/- 0.26 g/min (P less than 0.05) after acceleration of pulmonary edema. Kf was increased from initial values of 0.058 +/- 0.027 to 0.075 +/- 0.029 ml.min-1.mmHg-1 (P less than 0.05) after acceleration. In five additional dogs we cannulated lung lymphatics and determined the lymph to plasma protein concentration ratio (CL/CP) before and after acceleration. CL/CP increased from base-line values of 0.37 +/- 0.07 to 0.44 +/- 0.06 (P less than 0.05) after acceleration. Both the increase in Kf and CL/CP data support the hypothesis that acceleration of edema is due, in part, to a slight increase in microvascular membrane permeability. However, the findings could also have been caused by an increase in interstitial conductance, washout of interstitial proteins, or alveolar flooding.

Effect of systemic venous pressure elevation on lymph flow and lung edema formation

1986 ◽  
Vol 61 (5) ◽  
pp. 1634-1638 ◽  
Author(s):  
G. A. Laine ◽  
S. J. Allen ◽  
J. Katz ◽  
J. C. Gabel ◽  
R. E. Drake
Keyword(s):  
Pulmonary Edema ◽  
Superior Vena ◽  
Venous Pressure ◽  
Weight Ratio ◽  
Lymph Flow ◽  
Ratio Method ◽  
Positive Pressure ◽  
Fluid Accumulation ◽  
Edema Formation ◽  
Significant Difference

Pulmonary lymph drains into the thoracic duct and then into the systemic venous circulation. Since systemic venous pressure (SVP) must be overcome before pulmonary lymph can flow, variations in SVP may affect lymph flow rate and therefore the rate of fluid accumulation within the lung. The importance of this issue is evident when one considers the variety of clinical interventions that increase SVP and promote pulmonary edema formation, such as volume infusion, positive-pressure ventilation, and various vasoactive drug therapies. We recorded pulmonary arterial pressure (PAP), left atrial pressure (LAP), and SVP in chronic unanesthetized sheep. Occlusion balloons were placed in the left atrium and superior vena cava to control their respective pressures. The superior vena caval occluder was placed above the azygos vein so that bronchial venous pressure would not be elevated when the balloon was inflated. Three-hour experiments were carried out at various LAP levels with and without SVP being elevated to 20 mmHg. The amount of fluid present in the lung was determined by the wet-to-dry weight ratio method. At control LAP levels, no significant difference in lung fluid accumulation could be shown between animals with control and elevated SVP levels. When LAP was elevated above control a significantly greater amount of pulmonary fluid accumulated in animals with elevated SVP levels compared with those with control SVP levels. We conclude that significant excess pulmonary edema formation will occur when SVP is elevated at pulmonary microvascular pressures not normally associated with rapid fluid accumulation.

Mechanisms leading to lung edema in pulmonary embolization

1960 ◽  
Vol 198 (3) ◽  
pp. 543-546 ◽  
Author(s):  
S. A. Kabins ◽  
J. Fridman ◽  
J. Neustadt ◽  
G. Espinosa ◽  
L. N. Katz
Keyword(s):  
Pulmonary Edema ◽  
Capillary Permeability ◽  
Lysergic Acid ◽  
Lung Edema ◽  
Pulmonary Infarction ◽  
Edema Formation ◽  
Lung Lobe ◽  
Pulmonary Embolization ◽  
Sympathetic Nervous ◽  
Lung Lobes

A localized pulmonary infarction was produced by injecting a starch suspension into the pulmonary artery wedge position of one lung lobe in pentobarbitalized dogs, and the effect of three so-called antiserotonins on the ensuing pulmonary edema was determined. Edema was inhibited in the nonembolized lung lobes in 88% of the B.A.S. (1-benzyl-2-methyl-5-methoxytryptamine HCl), 45% of the DHE (dihydroergotamine), and 12% of the BOL (2-brom- d-lysergic acid diethylamide) dogs. Reasons are given for assuming that the actions of B.A.S. and DHE are due to their antiadrenergic rather than to any antiserotonin properties which they may have. Serotonin, therefore, at most has a slight role in the pulmonary edema formation caused by starch emboli. It is postulated that the emboli by producing an infarct and setting up a reflex mediated through the sympathetic nervous system, cause the release in turn of catecholamines and of histamine, the latter being immediately responsible for the capillary permeability change leading to pulmonary edema.

Alpha-thrombin-induced pulmonary vasoconstriction

1987 ◽  
Vol 63 (5) ◽  
pp. 1993-2000 ◽  
Author(s):  
M. J. Horgan ◽  
J. W. Fenton ◽  
A. B. Malik
Keyword(s):  
Pulmonary Edema ◽  
Base Line ◽  
Thrombin Injection ◽  
Weight Changes ◽  
Lung Weight ◽  
Edema Formation ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Hemodynamic ◽  
Proteolytic Site ◽  
Synthase Inhibitor

We examined the direct effects of thrombin on pulmonary vasomotor tone in isolated guinea pig lungs perfused with Ringer albumin (0.5% g/100 ml). The injection of alpha-thrombin (the native enzyme) resulted in rapid dose-dependent increases in pulmonary arterial pressure (Ppa) and pulmonary capillary pressure (Ppc), which were associated with an increase in the lung effluent thromboxane B2 concentration. The Ppa and Ppc responses decreased with time but then increased again within 40 min after thrombin injection. The increases in Ppc were primarily the result of postcapillary vasoconstriction. Pulmonary edema as evidenced by marked increases (60% from base line) in lung weight occurred within 90 min after thrombin injection. Injection of modified thrombins (i.e., gamma-thrombin lacking the fibrinogen recognition site or i-Pr2P-alpha-thrombin lacking the serine proteolytic site) was not associated with pulmonary hemodynamic or weight changes nor did they block the effects of alpha-thrombin. Indomethacin (a cyclooxygenase inhibitor), dazoxiben (a thromboxane synthase inhibitor), or hirudin (a thrombin antagonist) inhibited the thrombin-induced pulmonary vasoconstriction, as well as the pulmonary edema. We conclude that thrombin-induced pulmonary vasoconstriction is primarily the result of constriction of postcapillary vessels, and the response is mediated by generation of cyclooxygenase-derived metabolites. The edema formation is also dependent on activation of the cyclooxygenase pathway. The proteolytic site of alpha-thrombin is required for the pulmonary vasoconstrictor and edemogenic responses.

Effect of eicosanoid inhibition on the development of pulmonary edema after acute lung injury

1996 ◽  
Vol 80 (3) ◽  
pp. 915-923 ◽  
Author(s):  
D. P. Schuster ◽  
A. H. Stephenson ◽  
S. Holmberg ◽  
P. Sandiford
Keyword(s):  
Acute Lung Injury ◽  
Oleic Acid ◽  
Lung Injury ◽  
Pulmonary Edema ◽  
Experimental Models ◽  
Nuclear Medicine Imaging ◽  
Lung Water ◽  
Edema Formation ◽  
Cyclooxygenase Inhibition ◽  
Positron Emission

In experimental models of acute lung injury, cyclooxygenase inhibition improves oxygenation, presumably by causing a redistribution of blood flow away from edematous lung regions. This effect on perfusion pattern could also reduce alveolar edema formation. On the other hand, pulmonary pressures usually increase after cyclooxygenase inhibition, an effect that could exacerbate edema accumulation. Therefore we tested the following hypothesis: the total accumulation of pulmonary edema in dogs during a 24- to 28-h period of observation after acute lung injury caused by oleic acid will be less in a group of animals treated with meclofenamate (n = 6) or with the thromboxane-receptor blocker ONO-3708 (n = 5) than in a group of animals treated with oleic acid alone (placebo, n = 6). Lung water concentrations (LWC), the regional pattern of pulmonary perfusion, and protein permeability were measured with the nuclear medicine imaging technique of positron emission tomography. After 24-28 h, LWC was significantly less (P < 0.05) in the ONO-3708 group than in the meclofenamate group (a similar trend was seen compared with the placebo group, P = 0.12). After 24-28 h, pulmonary arterial pressures were highest in the meclofenamate group. Regardless of group, the only significant correlation with the change in LWC was with the integral of pulmonary pressures over the 24- to 28-h period. The data suggest that thromboxane inhibition will reduce edema accumulation in acute lung injury but that this effect depends on reducing as much as possible the simultaneous development of pulmonary hypertension from other causes.

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