Aerosolized Pseudomonas elastase and lung fluid balance in anesthetized sheep

1992 ◽  
Vol 72 (5) ◽  
pp. 1927-1933 ◽  
Author(s):  
B. T. Peterson ◽  
M. L. Collins ◽  
L. D. Gray ◽  
A. O. Azghani
Keyword(s):  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Water Volume ◽  
Lung Epithelium ◽  
Lung Water ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Lung Epithelial ◽  
Lung Epithelial Permeability

The role of the lung epithelium in lung fluid balance was studied by ventilating anesthetized sheep with an aerosol of 20 mg of elastase from Pseudomonas aeruginosa (Ps. elastase) to increase lung epithelial permeability without affecting lung endothelial permeability or lung vascular pressures. Ps. elastase had no effect on the lung vascular pressures, the alveolar-arterial PO2 gradient (A-aPO2), the flow or protein concentration of the lung lymph, or the postmortem water volume of the lungs. The morphological alveolar flooding score in these sheep was 2.5 times the control level, but this was only marginally significant. Elevation of the left atrial pressure by 20 cmH2O alone increased the postmortem lung water volume but had no effect on A-aPO2, the alveolar flooding score, or the lung epithelial permeability assessed by the clearance of 99mTc-labeled human serum albumin. Addition of aerosolized Ps. elastase to these sheep had no effect on the total lung water volume, but it caused a redistribution of water into the air spaces, as evidenced by significant increases in the alveolar flooding score and A-aPO2 (P less than 0.01). Elevation of the left atrial pressure by 40 cmH2O without elastase caused the same response as elevation of the left atrial pressure by 20 cmH2O with elastase, except the higher pressure caused a greater increase in the total lung water volume. We conclude that alteration of the integrity of the lung epithelium with aerosolized Ps. elastase causes a redistribution of lung water into the alveoli without affecting the total lung water volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Lung fluid balance during acute renal failure in sheep

1986 ◽  
Vol 60 (4) ◽  
pp. 1333-1340 ◽  
Author(s):  
B. T. Peterson ◽  
J. A. Brooks ◽  
R. W. Hyde
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Water Volume ◽  
Bilateral Nephrectomy ◽  
Lung Water ◽  
Lung Fluid ◽  
Protein Clearance

To determine whether uremia changes lung vascular permeability, we measured the flow of lymph and proteins from the lungs of acutely uremic sheep. Acute renal failure was induced by either bilateral nephrectomy or by reinfusing urine. Both models of renal failure increased the plasma creatinine from 0.8 +/- 0.3 to 11 +/- 1 mg/dl in 3 days but caused no significant change in the flow of lymph from the lungs. To determine whether uremia increased the protein clearance response to elevated pulmonary microvascular pressures, we inflated a balloon in the left atrium for 2 h before and 3 days after inducing acute renal failure. In seven sheep, before removing the kidneys, the 20 cmH2O elevation of left atrial pressure increased the protein clearance 3.9 +/- 3.0 ml/h (from 9.5 +/- 4.9 to 13.4 +/- 5.4 ml/h). Three days after the bilateral nephrectomy the same increase in left atrial pressure increased the protein clearance 6.4 +/- 3.6 ml/h (from 6.1 +/- 2.1 to 12.5 +/- 5.2 ml/h), which was a significantly larger increase than that measured before the nephrectomy (P less than 0.05). Sham nephrectomy in seven sheep caused the protein clearance response to the elevated left atrial pressure to fall from 4.7 +/- 1.9 ml/h before the sham nephrectomy to 2.6 +/- 1.4 ml/h 3 days later (P less than 0.05). Uremia due to reinfusion of urine in five sheep did not affect the protein clearance response to elevations in left atrial pressure. Neither model of acute uremia increased the postmortem extravascular lung water volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Correlation of Extravascular Lung Water with Cardiac Output and Left Atrial Pressure in Man

1976 ◽  
Vol 51 (3) ◽  
pp. 5P-6P
Author(s):  
C. G. C. MacArthur ◽  
C. G. Rhodes ◽  
F. Fazio ◽  
T. Jones ◽  
J. M. B. Hughes
Keyword(s):  
Cardiac Output ◽  
Extravascular Lung Water ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Lung Water

Specificity and sensitivity of noninvasive measurement of pulmonary vascular protein leak

1985 ◽  
Vol 59 (2) ◽  
pp. 564-574 ◽  
Author(s):  
I. M. Dauber ◽  
W. T. Pluss ◽  
A. VanGrondelle ◽  
R. S. Trow ◽  
J. V. Weil
Keyword(s):  
Lung Injury ◽  
Left Atrial ◽  
Low Dose ◽  
Gamma Probe ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
High Dose ◽  
Lung Water ◽  
Specificity And Sensitivity ◽  
Rate Of Increase

Noninvasive techniques employing external counting of radiolabeled protein have the potential for measuring pulmonary vascular protein permeability, but their specificity and sensitivity remain unclear. We tested the specificity and sensitivity of a double-radioisotope method by injecting radiolabeled albumin (131I) and erythrocytes (99mTc) into anesthetized dogs and measuring the counts of each isotope for 150 min after injection with an external gamma probe fixed over the lung. We calculated the rate of increase of albumin counts measured by the probe (which reflects the rate at which protein leaks into the extravascular space). To assess permeability we normalized the rate of increase in albumin counts for changes in labeled erythrocyte signal to minimize influence of changes in vascular surface area and thus derived an albumin leak index. We measured the albumin leak index and gravimetric lung water during hydrostatic edema (acutely elevating left atrial pressure by left atrial balloon inflation: mean pulmonary arterial wedge pressure = 22.6 Torr) and in lung injury edema induced by high- (1.0 g/kg) and low-dose (0.25 g/kg) intravenous thiourea. To test specificity we compared hydrostatic and high-dose thiourea edema. The albumin leak index increased nearly fourfold from control after thiourea injury (27.2 +/- 2.3 X 10–4 vs. 7.6 +/- 0.9 X 10–4 min-1) but did not change from control levels after elevating left atrial pressure (8.9 +/- 1.2 X 10–4 min-1) despite comparable increases in gravimetric lung water. To test sensitivity we compared low-dose thiourea with controls. Following low-dose thiourea, the albumin leak index nearly doubled despite the absence of a measurable increase in lung water. We conclude that a noninvasive double radioisotope measurement of pulmonary vascular protein leak, employing external counting techniques and a simplified method of calculation, is specific for lung injury and is also sensitive enough to detect lung injury insufficient to produce detectable pulmonary edema.

Effect of hypoproteinemia on lung fluid balance in awake newborn lambs

1986 ◽  
Vol 61 (3) ◽  
pp. 1139-1148 ◽  
Author(s):  
T. A. Hazinski ◽  
R. D. Bland ◽  
T. N. Hansen ◽  
E. G. Sedin ◽  
R. B. Goldberg
Keyword(s):  
Plasma Protein ◽  
Fluid Balance ◽  
Left Atrial ◽  
Protein Concentration ◽  
Lymph Flow ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Plasma Protein Concentration ◽  
Lung Fluid ◽  
Lung Lymph

To study the influence of plasma protein concentration on fluid balance in the newborn lung, we measured pulmonary arterial and left atrial pressures, lung lymph flow, and concentrations of protein in lymph and plasma of eight lambs, 2–3 wk old, before and after we reduced their plasma protein concentration from 5.8 +/- 0.3 to 3.6 +/- 0.6 g/dl. Each lamb underwent two studies, interrupted by a 3-day period in which we drained protein-rich systemic lymph through a thoracic duct fistula and replaced fluid losses with feedings of a protein-free solution of electrolytes and glucose. Each study consisted of a 2-h control period followed by 4 h of increased lung microvascular pressure produced by inflation of a balloon in the left atrium. Body weight and vascular pressures did not differ significantly during the two studies, but lung lymph flow increased from 2.6 +/- 0.1 ml/h during normoproteinemia to 4.1 +/- 0.1 ml/h during hypoproteinemia. During development of hypoproteinemia, the average difference in protein osmotic pressure between plasma and lymph decreased by 1.6 +/- 2 Torr at normal left atrial pressure and by 4.9 +/- 2.2 Torr at elevated left atrial pressure. When applied to the Starling equation governing microvascular fluid balance, these changes in liquid driving pressure were sufficient to account for the observed increases in lung fluid filtration; reduction of plasma protein concentration did not cause a statistically significant change in calculated filtration coefficient. Protein loss did not influence net protein clearance from the lungs nor did it accentuate the increase in lymph flow associated with left atrial pressure elevation.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of prolonged elevated microvascular pressure on lung fluid balance in sheep

1985 ◽  
Vol 58 (3) ◽  
pp. 869-875 ◽  
Author(s):  
R. E. Parker ◽  
R. J. Roselli ◽  
K. L. Brigham
Keyword(s):  
Arterial Pressure ◽  
Left Atrial ◽  
Systemic Arterial Pressure ◽  
Protein Fractions ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Base Line ◽  
Total Proteins ◽  
Lung Fluid ◽  
Osmotic Reflection Coefficient

Experiments were conducted in seven chronically instrumented unanesthetized sheep to estimate the osmotic reflection coefficient (sigma d) for total proteins and the solvent-drag reflection coefficients (sigma f) for six endogenous protein fractions. We measured the lymph-to-plasma ratio of total proteins (CL/CP) and six protein fractions during base-line conditions and after left atrial pressure elevations of 24–26 h per elevation. We also monitored pulmonary arterial pressure, left atrial pressure, systemic arterial pressure, and lung lymph flow at the various levels of pulmonary microvascular pressure. Our results indicate the CL/CP may require up to 24 h to reach a true steady state. It was found that sigma d is at least 0.89 for total proteins and sigma f is at least 0.84, 0.87, 0.86, 0.92, 0.95, and 0.96 for protein fractions with effective molecular radii of 36, 39.5, 44, 66, 105, and 123 A, respectively. In addition, the sigma f values for various protein fractions obtained from this investigation are compared with the predicted values of various mathematical models of the lung microcirculation.

High-frequency ventilation: lymph flow, lymph protein flux, and lung water

1984 ◽  
Vol 57 (1) ◽  
pp. 240-245 ◽  
Author(s):  
D. Martin ◽  
K. Rehder ◽  
J. C. Parker ◽  
A. E. Taylor
Keyword(s):  
High Frequency ◽  
Left Atrial ◽  
Plasma Proteins ◽  
Lymph Flow ◽  
Microvascular Permeability ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
High Frequency Ventilation ◽  
Total Plasma ◽  
Lung Water

The effects of high-frequency oscillatory (HFV) ventilation on lung fluid balance and microvascular permeability to macromolecules were measured in open-chest dog lungs. Prenodal lung lymph flow, concentration of total plasma proteins in lymph and plasma, pulmonary arterial and left atrial pressure,cardiac output, and blood-free lung wet-to-dry weight ratios were measured for conventional mechanical ventilation (CMV, 12/min, 200–300 ml tidal volume) and HFV of 15 Hz and a stroke volume of 40–50 ml for normal and elevated left atrial pressures. HFV increased both lymph flow and lung water (68 and 20%, respectively), and lymph-to-plasma ratios of total plasma proteins remained unchanged. When left atrial pressure was increased, an analysis of lymph protein flux indicates that the lung microvascular permeability was not altered by HFV. The increase in lymph flow and lung water associated with HFV may reflect an increased microvascular exchange surface area or a change in interstitial fluid pressure.

Lymph flow and lung weight in isolated sheep lungs

1986 ◽  
Vol 61 (5) ◽  
pp. 1830-1835 ◽  
Author(s):  
W. Mitzner ◽  
J. T. Sylvester
Keyword(s):  
Weight Gain ◽  
Arterial Pressure ◽  
Left Atrial ◽  
Pulmonary Arterial Pressure ◽  
Lymph Flow ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Lung Water ◽  
Lung Weight ◽  
Pulmonary Arterial

To study the relationship between lung weight and lymph flow, we used an in situ, isolated sheep lung preparation that allowed these two variables to be measured simultaneously. All lungs were perfused for 4.5 h at a constant rate of 100 ml X min-1 X kg-1. In control lungs, the left atrial pressure (Pla) was kept at atmospheric pressure. In experimental lungs, Pla was kept atmospheric except for a 50-min elevation to 18 mmHg midway through the perfusion. During this period of left atrial hypertension, pulmonary arterial pressure rose from 18 to 31 mmHg, lymph flow rose from 3 to 12 ml/h, and the lymph-to-plasma oncotic pressure ratio (pi L/pi P) fell from 0.7 to 0.48. After left atrial pressure was returned to control, pulmonary arterial pressure, lymph flow, and pi L/pi P all returned to control levels. The rate of weight gain after the return of left atrial pressure to control was also the same as that in the control group. However, during the period of left atrial hypertension 135 ml of fluid were filtered into the lung, and this large increase in lung weight remained after the pressure was lowered. The presence of this substantial excess lung water despite control values for vascular pressures, lymph flow, rate of weight gain, and pi L/pi P suggests that the absolute amount of lung water has little influence on the dynamic aspects of lung fluid balance. These results are consistent with a two-compartment model of the interstitial space, where only one of the compartments is readily drained by the lymphatics.

Responses of pulmonary C-fibre and rapidly adapting receptor afferents to pulmonary congestion and edema in dogs

1992 ◽  
Vol 70 (1) ◽  
pp. 68-76 ◽  
Author(s):  
K. Ravi ◽  
C. T. Kappagoda
Keyword(s):  
Pulmonary Edema ◽  
Extravascular Lung Water ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Lung Water ◽  
Control Value ◽  
Significant Stimulation ◽  
C Fibre ◽  
The Mean

The effects of cardiogenic and noncardiogenic pulmonary edema on the activities of rapidly adapting receptors (RARs) and pulmonary C-fibre receptors were investigated in dogs anaesthetized with chloralose. Cardiogenic pulmonary edema was produced by elevating the mean left atrial pressure by 25 mmHg (1 mmHg = 133.32 Pa) above the control value for a period of 45 min, by partial obstruction of the mitral valve. Noncardiogenic pulmonary edema was produced by injecting alloxan (100 mg/kg) intravenously. The effect of the latter was examined on RARs alone. Cardiogenic edema activated RARs (n = 8) and the activity was greatest during the first few minutes after elevation of mean left atrial pressure. The pulmonary C-fibre receptors (n = 6) were also activated by cardiogenic edema, but these responses were variable. Noncardiogenic pulmonary edema also activated RAR (n = 6), and this response was maintained during the entire recording period (20 min). The extravascular lung water (%), measured 15 min (n = 5) and 45 min (n = 5) after the elevation of the mean left atrial pressure, was significantly elevated above control values. However, these two values were not significantly different from each other. The extravascular lung water increased significantly after the injection of alloxan also (n = 5). These results show that during pulmonary edema, there is significant stimulation of the RARs and the pulmonary C-fibre receptors. It is suggested that the reflex respiratory responses observed in pulmonary edema may be due to the activation of both the RARs and the pulmonary C-fibre receptors.Key words: alloxan, cardiogenic edema, vagus.

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