Dynamic Insufficiency of Lung Lymph Flow from the Right Lymph Duct in Dogs with Acute Filtration Edema1,2

1983 ◽  
Vol 127 (1) ◽  
pp. 67-71 ◽  
Author(s):  
Kazuya Nakahara ◽  
Satoru Nanjo ◽  
Masazumi Maeda ◽  
Yasunaru Kawashima
Keyword(s):  
Lymph Flow ◽  
Lymph Duct ◽  
The Right ◽  
Lung Lymph ◽  
Lung Lymph Flow

Unilateral smoke inhalation in sheep: effect on left lung lymph flow with right lung injury

1996 ◽  
Vol 271 (6) ◽  
pp. R1620-R1624 ◽  
Author(s):  
Y. Kikuchi ◽  
L. D. Traber ◽  
D. N. Herndon ◽  
D. L. Traber
Keyword(s):  
Reflection Coefficient ◽  
Pulmonary Veins ◽  
Left Lung ◽  
Lymph Flow ◽  
Microvascular Permeability ◽  
Smoke Inhalation ◽  
Fourfold Increase ◽  
The Right ◽  
Lung Lymph ◽  
Lung Lymph Flow

We previously reported that smoke inhalation to the right lung will result in damage to the air-insufflated left lung. In this study we confirm these findings and determine whether this injury is associated with an elevation in lung lymph flow and pulmonary microvascular permeability to protein as indexed by changes in reflection coefficient. Sheep (n = 12) were surgically prepared by placement of a Swan-Ganz catheter and pneumatic occluders on all pulmonary veins and the left pulmonary artery. The left lung lymphatic was selectively cannulated as shown previously (Y. Kikuchi, H. Nakazawa, and D. Traber. Am. J. Physiol. 269 (Regulatory Integrative Comp. Physiol. 38): R943-R947, 1995). All afferent lymphatics from the right lung were severed, and the right pulmonary ligament was sectioned. The caudal end of the lymph node was sectioned to remove systemic lymph contamination. The sheep were studied in the unanesthetized state 7 days later. To ensure that lymph flow was exclusively from the left lung (QLL), right pulmonary microvascular pressure was increased, a procedure that resulted in little or no change in QLL, as was previously shown. The sheep were then anesthetized, and a Carlens tube was positioned to allow separate ventilation of the right and left lung. The right lungs of five sheep and the left lungs of two sheep were insufflated with cotton smoke. Insufflation of the left lung with cotton smoke produced a fourfold increase in QLL that began 4 h after insult. Insufflation of the right lung with smoke led to a doubling of QLL that began 12 h after insult. Changes in QLL were associated with increased microvascular permeability, as indexed by the reflection coefficient. Control sheep (air insufflated into both lungs, n = 5) showed no change in QLL. Injury to the right lung resulted in damage to the left air-insufflated lung, suggesting a hematogenous mediation of the response.

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

1977 ◽  
Vol 43 (5) ◽  
pp. 894-898 ◽  
Author(s):  
C. E. Vreim ◽  
K. Ohkuda ◽  
N. C. Staub
Keyword(s):  
Pulmonary Edema ◽  
Thoracic Duct ◽  
Lymphatic Drainage ◽  
Lymph Flow ◽  
Base Line ◽  
Anesthetized Dogs ◽  
Lymph Duct ◽  
Lung Lymph ◽  
Severe Pulmonary Edema ◽  
Lung Lymph Flow

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.

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.

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