Pulmonary Air Embolization Inhibits Lung Lymph Flow by Increasing Lymphatic Outflow Pressure

2006 ◽  
Vol 4 (1) ◽  
pp. 18-22 ◽  
Author(s):  
Randolph H. Stewart ◽  
Christopher M. Quick ◽  
David C. Zawieja ◽  
Charles S. Cox ◽  
Steven J. Allen ◽  
...  
Keyword(s):  
Lymph Flow ◽  
Lung Lymph ◽  
Lung Lymph Flow

Role of anti-L-selectin antibody in burn and smoke inhalation injury in sheep

2002 ◽  
Vol 283 (5) ◽  
pp. L1043-L1050 ◽  
Author(s):  
Jiro Katahira ◽  
Kazunori Murakami ◽  
Frank C. Schmalstieg ◽  
Robert Cox ◽  
Hal Hawkins ◽  
...  
Keyword(s):  
Leukocyte Adhesion ◽  
Experimental Period ◽  
Inhalation Injury ◽  
Lymph Flow ◽  
Smoke Inhalation ◽  
Control Group ◽  
Fluid Flux ◽  
Smoke Inhalation Injury ◽  
Lung Lymph ◽  
Lung Lymph Flow

We hypothesized that the antibody neutralization of L-selectin would decrease the pulmonary abnormalities characteristic of burn and smoke inhalation injury. Three groups of sheep ( n = 18) were prepared and randomized: the LAM-(1–3) group ( n = 6) was injected intravenously with 1 mg/kg of leukocyte adhesion molecule (LAM)-(1-3) (mouse monoclonal antibody against L-selectin) 1 h after the injury, the control group ( n = 6) was not injured or treated, and the nontreatment group ( n = 6) was injured but not treated. All animals were mechanically ventilated during the 48-h experimental period. The ratio of arterial Po 2 to inspired O2 fraction decreased in the LAM-(1–3) and nontreatment groups. Lung lymph flow and pulmonary microvascular permeability were elevated after injury. This elevation was significantly reduced when LAM-(1–3) was administered 1 h after injury. Nitrate/nitrite (NO x ) amounts in plasma and lung lymph increased significantly after the combined injury. These changes were attenuated by posttreatment with LAM-(1–3). These results suggest that the changes in pulmonary transvascular fluid flux result from injury of lung endothelium by polymorphonuclear leukocytes. In conclusion, posttreatment with the antibody for L-selectin improved lung lymph flow and permeability index. L-selectin appears to be principally involved in the increased pulmonary transvascular fluid flux observed with burn/smoke insult. L-selectin may be a useful target in the treatment of acute lung injury after burn and smoke inhalation.

Hypobaric hypoxia does not affect lung fluid or protein exchange in awake adult sheep at rest

1983 ◽  
Vol 61 (7) ◽  
pp. 714-716
Author(s):  
G. Coates ◽  
L. W. Belbeck ◽  
G. W. Gray
Keyword(s):  
Pulmonary Artery ◽  
Left Atrial ◽  
Hypobaric Hypoxia ◽  
Barometric Pressure ◽  
Lymph Flow ◽  
Adult Sheep ◽  
Lung Fluid ◽  
Lung Lymph ◽  
Lung Lymph Flow ◽  
Protein Exchange

We measured pulmonary artery [Formula: see text] and left atrial [Formula: see text] pressures, lung lymph flow, and lymph/plasma protein concentrations in four adult sheep at a barometric pressure of 380 Torr (1 Torr = 133.322 Pa) for 22 h. Hypobaric hypoxia caused an immediate increase in [Formula: see text] from 20 to 39 Torr. There was no significant change in [Formula: see text], lymph flow, or lymph protein concentrations. We conclude that hypobaric hypoxia does not affect lung fluid or protein exchange in awake adult sheep at rest.

scholarly journals Effects of tidal volume and respiratory frequency on lung lymph flow

2005 ◽  
Vol 99 (2) ◽  
pp. 556-563 ◽  
Author(s):  
David B. Pearse ◽  
Robert M. Searcy ◽  
Wayne Mitzner ◽  
Solbert Permutt ◽  
J. T. Sylvester
Keyword(s):  
Tidal Volume ◽  
Lymphatic Vessels ◽  
Lymph Flow ◽  
Edema Formation ◽  
Fluid Filtration ◽  
Induced Changes ◽  
Lung Lymph ◽  
Lung Lymph Flow

Ventilation (V̇) increases lung lymph flow (Q̇l), but the separate effects of tidal volume (Vt) and frequency (f) and the role of V̇-induced changes in edema formation are poorly understood. An isolated, in situ sheep lung preparation was used to examine these effects. In eight sheep with f = 10 min−1, results obtained during 30-min periods with Vt = 5 or 20 ml/kg were compared with values obtained during bracketed 30-min control periods (Vt = 12.5 ml/kg). Eight other sheep with constant Vt (12.5 ml/kg) were studied at f = 5 or 20 min−1 and compared with f = 10 min−1. Three additional groups of six sheep were perfused for 100 min with control V̇ (10 ml/kg, 10 min−1). Vt was then kept constant or changed to 20 or 3 ml/kg during a second 100-min period. Increases in Vt or f increased Q̇l and vice versa, without corresponding effects on the rate of edema formation. For the same change in V̇, changing Vt had a greater effect on Q̇l than changing f. The change in Q̇l caused by an increase in Vt was significantly greater after the accumulation of interstitial edema. The change in Q̇l caused by a sustained increase in Vt was transient and did not correlate with the rate of edema formation, suggesting that V̇ altered Q̇l through direct mechanical effects on edema-filled compartments and lymphatic vessels rather than through V̇-induced changes in fluid filtration.

Plasma tumor necrosis factor-alpha during long-term endotoxemia in awake sheep

1992 ◽  
Vol 73 (5) ◽  
pp. 1831-1837 ◽  
Author(s):  
P. J. Sloane ◽  
T. H. Elsasser ◽  
J. A. Spath ◽  
K. H. Albertine ◽  
M. H. Gee
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Lymph Flow ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Endotoxin Infusion ◽  
Factor Alpha ◽  
Lung Lymph ◽  
Necrosis Factor ◽  
Lung Lymph Flow

We used a continuous 12-h infusion of Escherichia coli endotoxin (10 ng.min-1.kg-1) in 10 awake sheep equipped with a lung lymph fistula and vascular catheters to determine the time course of increased plasma tumor necrosis factor-alpha (TNF-alpha) during the infusion and a 12-h postinfusion period. Lung lymph flow increased progressively during the infusion to a peak value averaging 8.6 +/- 2.0 times the baseline flow of 6.3 +/- 1.3 g/h. During the postinfusion period, lung lymph flow remained elevated at three to four times baseline. The lymph-to-plasma protein concentration ratio was unchanged from baseline over 24 h, indicating a dramatic increase in net protein flux across pulmonary microvessels. The TNF-alpha concentration peaked early in the infusion and then declined, despite the continuing presence of endotoxin. Plasma TNF-alpha concentration increased 10-fold (0.33 +/- 0.05 ng/ml at baseline to 3.89 +/- 0.78 ng/ml peak) 2 h into the endotoxin infusion. At the end of the endotoxin infusion, plasma TNF-alpha had decreased to 1.16 +/- 0.19 ng/ml. The circulating TNF-alpha concentration did not correlate with pathophysiology or outcome in these sheep.

Effect of endotoxin on airway responsiveness to aerosol histamine in sheep

1983 ◽  
Vol 54 (6) ◽  
pp. 1463-1468 ◽  
Author(s):  
A. A. Hutchison ◽  
J. M. Hinson ◽  
K. L. Brigham ◽  
J. R. Snapper
Keyword(s):  
Dynamic Compliance ◽  
Airway Responsiveness ◽  
Lymph Flow ◽  
Lung Mechanics ◽  
Whole Body ◽  
Base Line ◽  
Residual Capacity ◽  
Induced Changes ◽  
Lung Lymph ◽  
Lung Lymph Flow

This study tested the hypothesis that in the awake sheep, airway responsiveness to aerosol histamine would be increased acutely by endotoxemia. Eleven sheep were chronically instrumented to allow for measurements of lung lymph flow, vascular pressures, and lung mechanics. Awake sheep were studied in a whole-body plethysmograph designed to measure dynamic compliance (Cdyn), resistance of the lung (RL), and functional residual capacity (FRC). Pulmonary responsiveness to aerosol histamine was assessed by giving five breaths of increasing concentrations of histamine (0.1–50 mg/ml) until Cdyn decreased to 65% (of control) or until 50 mg/ml of histamine had been given. Escherichia coli endotoxin (0.2–0.5 microgram/kg) was then infused, and at 5 h after endotoxemia pulmonary responsiveness to aerosol histamine was remeasured. After endotoxin, 9 of the 11 sheep exhibited decreased Cdyn at a lower concentration of histamine compared with the preendotoxin level (P less than 0.05). The mean of the log dose of histamine necessary to reduce Cdyn to 65% of control was 1.00 +/- 0.16 (SE) before endotoxin and 0.027 +/- 0.29 5 h after endotoxin; i.e., histamine responsiveness was increased. In the last 3 sheep studied, atropine (0.1 mg/kg iv) was given after the second aerosol histamine challenge, and a third dose-response curve was performed. Atropine did not return the endotoxin-induced increase in histamine responsiveness to base line. There was no correlation between the change in histamine responsiveness and the endotoxin-induced changes in Cdyn, FRC, RL, alveolar-arterial O2 difference, pulmonary arterial pressure, or lung lymph flow.

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

1978 ◽  
Vol 42 (4) ◽  
pp. 550-557 ◽  
Author(s):  
W C Woolverton ◽  
K L Brigham ◽  
N C Staub
Keyword(s):  
Water Content ◽  
Lymph Flow ◽  
Positive Pressure ◽  
Lung Lymph ◽  
Lung Lymph Flow

Effect of interstitial edema on lung lymph flow in goats in the absence of filtration

1992 ◽  
Vol 72 (3) ◽  
pp. 1142-1148 ◽  
Author(s):  
K. Kambara ◽  
K. E. Longworth ◽  
V. B. Serikov ◽  
N. C. Staub
Keyword(s):  
Lymph Flow ◽  
Alveolar Wall ◽  
Half Time ◽  
Interstitial Edema ◽  
Lung Water ◽  
Pulmonary Arterial ◽  
The Mean ◽  
Lung Lymph ◽  
Normal Lungs ◽  
Lung Lymph Flow

We tested the effect of interstitial edema on lung lymph flow when no filtration occurred. In 16 anesthetized open-thorax ventilated supine goats, we set pulmonary arterial and left atrial pressures to nearly zero and measured lymph flow for 3 h from six lungs without edema and ten with edema. Lymph flow decreased exponentially in all experiments as soon as filtration ceased. In the normal lungs the mean half time of the lymph flow decrease was 12.7 +/- 4.8 (SD) min, which was significantly shorter (P less than 0.05) than the 29.1 +/- 14.8 min half time in the edematous lungs. When ventilation was stopped, lymph flow in the edematous lungs decreased as rapidly as in the normal lungs. The total quantity of lymph after filtration ceased was 2.7 +/- 0.8 ml in normal lungs and 9.5 +/- 6.3 ml in edematous lungs, even though extravascular lung water was doubled in the latter (8.4 +/- 2.4 vs. 3.3 +/- 0.4 g/g dry lung, P less than 0.01). Thus the maximum possible clearance of the interstitial edema liquid by the lymphatics was 6.3 +/- 4.8%. When we restarted pulmonary blood flow after 1–2 h in four additional goats, lymph flow recovered within 30 min to the baseline level. These findings support the hypothesis that lung lymph flow originates mainly from alveolar wall perimicrovascular interstitial liquid and that the contribution of the lung lymphatic system to the clearance of interstitial edema (bronchovascular cuffs, interlobular septa) is small.

Permeability of barriers to albumin flux in lungs of sheep resuscitated from hemorrhagic shock

1986 ◽  
Vol 61 (6) ◽  
pp. 2156-2161 ◽  
Author(s):  
A. B. Gorin ◽  
G. Mendiondo
Keyword(s):  
Hemorrhagic Shock ◽  
Extravascular Lung Water ◽  
Weight Ratio ◽  
Equilibrium Concentration ◽  
Dry Weight ◽  
Lymph Flow ◽  
Base Line ◽  
Lung Water ◽  
Lung Lymph ◽  
Lung Lymph Flow

We assessed pulmonary endothelial and epithelial permeability and lung lymph flow in nine adult sheep under base-line conditions and after resuscitation from profound hemorrhagic shock. Animals were mechanically ventilated and maintained on 1% halothane anesthesia while aortic pressure was held at 40 Torr for 3 h. Systemic heparin was not used. After reinfusion of shed blood, sheep recovered from anesthesia and we measured lung lymph flow (QL), lymph-to-plasma concentration ratio for proteins, and time taken to reach half-equilibrium concentration of intravenous tracer albumin in lymph (t1/2). Twenty-four hours after bolus injection of radio-albumin we lavaged subsegments of the right upper lobe and determined fractional equilibration of the tracer in the alveolar luminal-lining layer. In each sheep we had measured these parameters 7 days earlier under base-line conditions. Animals were killed, and the lungs were used for gravimetric determination of extravascular lung water (gravimetric extravascular lung water-to-dry weight ratio) 24 h after resuscitation from shock. Pulmonary endothelial injury after resuscitation was evidenced by marked increase in QL, without fall in lymph-to-plasma ratio. Time taken to reach half-equilibrium concentration fell from 169 +/- 47 (SD) min in base-line studies to 53 +/- 33 min after shock. There was no evidence of lung epithelial injury. Gravimetric extravascular lung water-to-dry weight ratio was significantly increased in these animals killed 24 h after resuscitation (4.94 +/- 0.29) compared with values in our laboratory controls (4.13 +/- 0.09, mean +/- SD). These data demonstrate a loss of lung endothelial integrity in sheep after resuscitation from profound hemorrhagic shock.

Furosemide reduces lung fluid filtration in lambs with lung microvascular injury from air emboli

1989 ◽  
Vol 67 (5) ◽  
pp. 1990-1996 ◽  
Author(s):  
M. E. Berner ◽  
W. G. Teague ◽  
R. G. Scheerer ◽  
R. D. Bland
Keyword(s):  
Cardiac Output ◽  
Left Atrial ◽  
Balloon Catheter ◽  
Lymph Flow ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Protein Ratio ◽  
Fluid Filtration ◽  
Lung Lymph ◽  
Lung Lymph Flow

To study the effects of furosemide on the neonatal pulmonary circulation in the presence of lung injury, we measured pulmonary arterial and left atrial pressures, cardiac output, lung lymph flow, and concentrations of protein in lymph and plasma of nine lambs that received furosemide, 2 mg/kg iv, during a continuous 8-h intravenous infusion of air. Air embolism increased pulmonary vascular resistance by 71% and nearly tripled steady-state lung lymph flow, with no change in lymph-to-plasma protein ratio. These findings reflect an increase in lung vascular protein permeability. During sustained lung endothelial injury, diuresis from furosemide led to a rapid reduction in cardiac output (average 29%) and a 2-Torr decrease in left atrial pressure. Diuresis also led to hemoconcentration, with a 15% increase in both plasma and lymph protein concentrations. These changes were associated with a 27% reduction in lung lymph flow. In a second set of studies, we prevented the reduction in left atrial pressure after furosemide by inflating a balloon catheter in the left atrium. Nevertheless, lymph flow decreased by 25%, commensurate with the reduction in cardiac output that occurred after furosemide. In a third series of experiments, we minimized the furosemide-related decrease in cardiac output by opening an external fistula between the carotid artery and jugular vein immediately after injection of furosemide. In these studies, the reduction in lung lymph flow (average 17%) paralleled the smaller (17%) decrease in cardiac output. These results suggest that changes in lung vascular filtration pressure probably do not account for the reduction in lung lymph flow after furosemide in the presence of lung vascular injury.(ABSTRACT TRUNCATED AT 250 WORDS)

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