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.

Lung lymph flow during volume infusions

1986 ◽  
Vol 60 (2) ◽  
pp. 623-629 ◽  
Author(s):  
J. C. Gabel ◽  
K. D. Fallon ◽  
G. A. Laine ◽  
R. E. Drake
Keyword(s):  
Venous Pressure ◽  
Ringer Solution ◽  
Lymph Flow ◽  
Lymph Vessel ◽  
Base Line ◽  
Crystalloid Solution ◽  
Lymph Vessels ◽  
Anesthetized Dogs ◽  
Lung Lymph ◽  
Lung Lymph Flow

We investigated the effect of intravenous isotonic crystalloid solution infusion on lung lymph flow. Tracheobronchial lung lymph vessels were cannulated in 13 anesthetized dogs. The lymph flow rate was measured 1) with the lymph flowing against atmospheric pressure (QL), and 2) with the pressure at the outflow end of the lymph cannula equal to systemic venous pressure (QLV). QL and QLV were measured alternately in each lymph vessel. In one group of nine dogs, the base-line QL and QLV were 18 +/- 9 and 13 +/- 6 (SD) microliter/min, respectively (P less than 0.05). QL increased by 4.8 +/- 1.4-fold, and QLV increased by 3.5 +/- 2.1-fold during a 4-h infusion of 25 ml X kg-1 X h-1 of Ringer solution. QLV was significantly less than QL at all times. The increases in lymph flow were caused primarily by a reduction in the effective resistance of the lymph vessels with little rise in the pressure driving lymph from the lungs. Because QLV flowed against systemic venous pressure, the increase in QLV was blunted by a 3.1 +/- 2.3 cmH2O rise in venous pressure during the infusions. In the remaining four dogs, we infused Ringer solution rapidly in order to raise venous pressure to greater than 15 cmH2O. This caused QL to increase by 25 +/- 7-fold; however, QLV decreased to zero. We conclude that elevations in venous pressure which occur during volume infusions oppose lung lymph flow and lead to accumulation of excess fluid in the lungs.

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.

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.

Effect of progressive exercise on lung fluid balance in sheep

1988 ◽  
Vol 64 (5) ◽  
pp. 2125-2131 ◽  
Author(s):  
J. H. Newman ◽  
B. J. Butka ◽  
R. E. Parker ◽  
R. J. Roselli
Keyword(s):  
Cardiac Output ◽  
Fluid Balance ◽  
Lymph Flow ◽  
Base Line ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Progressive Exercise ◽  
Pulmonary Arterial ◽  
Lung Lymph ◽  
Lung Lymph Flow

The purpose of this study is to determine the roles of cardiac output and microvascular pressure on changes in lung fluid balance during exercise in awake sheep. We studied seven sheep during progressive treadmill exercise to exhaustion (10% grade), six sheep during prolonged constant-rate exercise for 45–60 min, and five sheep during hypoxia (fraction of inspired O2 = 0.12) and hypoxic exercise. We made continuous measurements of pulmonary arterial, left atrial, and systemic arterial pressures, lung lymph flow, and cardiac output. Exercise more than doubled cardiac output and increased pulmonary arterial pressures from 19.2 +/- 1 to 34.8 +/- 3.5 (SE) cmH2O. Lung lymph flow increased rapidly fivefold during progressive exercise and returned immediately to base-line levels when exercise was stopped. Lymph-to-plasma protein concentration ratios decreased slightly but steadily. Lymph flows correlated closely with changes in cardiac output and with calculated microvascular pressures. The drop in lymph-to-plasma protein ratio during exercise suggests that microvascular pressure rises during exercise, perhaps due to increased pulmonary venous pressure. Lymph flow and protein content were unaffected by hypoxia, and hypoxia did not alter the lymph changes seen during normoxic exercise. Lung lymph flow did not immediately return to base line after prolonged exercise, suggesting hydration of the lung interstitium.

Effects of hypoproteinemia on lung microvascular protein sieving and lung lymph flow

1986 ◽  
Vol 60 (4) ◽  
pp. 1293-1299 ◽  
Author(s):  
R. E. Parker ◽  
N. E. Wickersham ◽  
R. J. Roselli ◽  
T. R. Harris ◽  
K. L. Brigham
Keyword(s):  
Total Protein ◽  
Protein Concentration ◽  
Lymph Flow ◽  
Reflection Coefficients ◽  
Base Line ◽  
Total Protein Concentration ◽  
Total Proteins ◽  
Osmotic Reflection Coefficient ◽  
Lung Lymph ◽  
Lung Lymph Flow

Experiments were conducted on five chronically instrumented unanesthetized sheep to determine the effects of sustained hypoproteinemia on lung fluid balance. Plasma total protein concentration was decreased from a control value of 6.17 +/- 0.019 to 3.97 +/- 0.17 g/dl (mean +/- SE) by acute plasmapheresis and maintained at this level by chronic thoracic lymph duct drainage. We measured pulmonary arterial pressure, left atrial pressure, aortic pressure, central venous pressure, cardiac output, oncotic pressures of both plasma and lung lymph, lung lymph flow rate, and lung lymph-to-plasma ratio of total proteins and six protein fractions for both control base-line conditions and hypoproteinemia base-line conditions. Moreover, we estimated the average osmotic reflection coefficient for total proteins and the solvent drag reflection coefficients for the six protein fractions during hypoproteinemia. Hypoproteinemia caused significant decreases in lung lymph total protein concentration, lung lymph-to-plasma total protein concentration ratio, and oncotic pressures of plasma and lung lymph. There were no significant alterations in the vascular pressures, lung lymph flow rate, cardiac output, or oncotic pressure gradient. The osmotic reflection coefficient for total proteins was found to be 0.900 +/- 0.004 for hypoproteinemia conditions, which is equal to that found in a previous investigation for sheep with a normal plasma protein concentration. Our results suggest that hypoproteinemia does not alter the lung filtration coefficient nor the reflection coefficients for plasma proteins. Possible explanations for the reported increase in the lung filtration coefficient during hypoproteinemia by other investigators are also made.

Effects of increased ventilation on lung lymph flow in unanesthetized sheep

1986 ◽  
Vol 60 (6) ◽  
pp. 2063-2070 ◽  
Author(s):  
S. M. Albelda ◽  
J. H. Hansen-Flaschen ◽  
P. N. Lanken ◽  
A. P. Fishman
Keyword(s):  
Cardiac Output ◽  
Dead Space ◽  
Total Protein ◽  
Minute Ventilation ◽  
Fluid Pressure ◽  
Lymph Flow ◽  
Base Line ◽  
Arterial Blood ◽  
Lung Lymph ◽  
Lung Lymph Flow

To determine the effect of an increase in spontaneous minute ventilation on lung fluid balance, we added external dead space to the breathing circuit of six tracheostomized, unanesthetized, spontaneously breathing sheep in which lung lymph fistulas had been created surgically. The addition of 120–180 ml of dead space caused minute ventilation to increase by 50–100% (secondary to increases in both tidal volume and frequency), without changing pulmonary arterial pressure, pulmonary capillary wedge pressure, cardiac output, or arterial blood gas tensions. The increase in spontaneous ventilation was associated with an average increase of 27% in lung lymph flow (P less than 0.05) and an average reduction of 11% in the lymph-to-plasma concentration ratio (L/P) for total protein (P less than 0.05). Lymph flow and L/P for total protein approached stable values after 2–3 h of hyperpnea, and the increase in lymph flow persisted for at least 18 h of dead-space breathing. Removal of dead space was associated with a rapid return (within 45 min) of lymph flow to base-line levels. These results suggest that hyperpnea increases the pulmonary transvascular filtration rate. Since no changes in vascular pressures or cardiac output were observed, this increase in transvascular filtration is most likely due to a fall in interstitial fluid pressure.

Oleic acid lung injury in sheep

1986 ◽  
Vol 60 (2) ◽  
pp. 433-440 ◽  
Author(s):  
M. Julien ◽  
J. M. Hoeffel ◽  
M. R. Flick
Keyword(s):  
Oleic Acid ◽  
Lung Injury ◽  
Pulmonary Edema ◽  
Fluid Balance ◽  
Lymph Flow ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Pulmonary Arterial ◽  
Lung Lymph ◽  
Lung Lymph Flow

Intravenous infusion of oleic acid into experimental animals causes acute lung injury resulting in pulmonary edema. We investigated the mechanism of oleic acid lung injury in sheep. In experiments with anesthetized and unanesthetized sheep with lung lymph fistulas, we measured pulmonary arterial and left atrial pressures, cardiac output, lung lymph flow, and lymph and plasma protein concentrations. We injured the lungs with intravenous infusions of oleic acid at doses ranging from 0.015 to 0.120 ml/kg. We found that oleic acid caused reproducible dose-related increases in pulmonary arterial pressure and pulmonary vascular resistance, arterial hypoxemia, and increased protein-rich lung lymph flow and extravascular lung water. The lung fluid balance changes were characteristic of increased permeability pulmonary edema. Infusion of the esterified fat triolein had no hemodynamic or lung fluid balance effects. Depletion of leukocytes with a nitrogen mustard or platelets with an antiplatelet serum had no effect on oleic acid lung injury. Treatment of sheep before injury with methylprednisolone 30 mg/kg or ibuprofen 12.5–15.0 mg/kg also had no effects. Unlike other well-characterized sheep lung injuries, injury caused by oleic acid does not require participation of leukocytes.

Pulmonary and coronary endothelial effects of acute myocardial ischemia in dogs

1982 ◽  
Vol 242 (3) ◽  
pp. H337-H348
Author(s):  
M. H. Gee ◽  
J. T. Flynn ◽  
J. A. Spath
Keyword(s):  
Steady State ◽  
Lymph Flow ◽  
Flow Rates ◽  
Protein Clearance ◽  
Acute Mi ◽  
Anesthetized Dogs ◽  
Pulmonary Arterial ◽  
Lung Lymph ◽  
Lung Vascular Permeability ◽  
Lung Lymph Flow

We measured pulmonary arterial (Ppa) and left atrial (Pla) pressures, lung lymph flow rate (QL), and protein clearance in 23 anesthetized dogs with ligation (MI) dogs or sham ligation (sham-MI dogs) of a coronary artery combined with either large transient increases in Pla or moderate steady-state increases in Pla. In steady-state experiments we also collected cardiac lymph. Plasma and lymph concentrations of several prostanoids including prostacyclin (PGI2) and thromboxane B2 (TXB2) were measured. Lung lymph flow rates and protein clearances were increased in MI dogs compared with those in sham-MI dogs in experiments with transient increases in Pla. Similarly in steady-state experiments lung QL and protein clearance were increased after MI. Cardiac QL increased after MI with no change in lymph protein clearance. Lung and cardiac lymph PGI2 and plasma TXB2 concentrations increased after MI. We suggest that acute MI results in increased lung vascular permeability and that activation of formed elements in blood may be involved in mediating MI-induced vascular injury.

Effects of inspiratory resistance loading on lung fluid balance in awake sheep

1986 ◽  
Vol 60 (1) ◽  
pp. 198-203 ◽  
Author(s):  
J. E. Loyd ◽  
K. B. Nolop ◽  
R. E. Parker ◽  
R. J. Roselli ◽  
K. L. Brigham
Keyword(s):  
Fluid Balance ◽  
Intrathoracic Pressure ◽  
Lymph Flow ◽  
Base Line ◽  
Plasma Protein Concentration ◽  
Lung Fluid ◽  
Mean Pulmonary Arterial Pressure ◽  
Lung Fluid Balance ◽  
Lung Lymph ◽  
Lung Lymph Flow

Because pulmonary edema has been associated clinically with airway obstruction, we sought to determine whether decreased intrathoracic pressure, created by selective inspiratory obstruction, would affect lung fluid balance. We reasoned that if decreased intrathoracic pressure caused an increase in the transvascular hydrostatic pressure gradient, then lung lymph flow would increase and the lymph-to-plasma protein concentration ratio (L/P) would decrease. We performed experiments in six awake sheep with chronic lung lymph cannulas. After a base-line period, we added an inspiratory load (20 cmH2O) and allowed normal expiration at atmospheric pressure. Inspiratory loading was associated with a 12-cmH2O decrease in mean central airway pressure. Mean left atrial pressure fell 11 cmH2O, and mean pulmonary arterial pressure was unchanged; calculated microvascular pressure decreased 8 cmH2O. The changes that occurred in lung lymph were characteristic of those seen after other causes of increased transvascular hydrostatic gradient, such as increased intravascular pressure. Lung lymph flow increased twice base line, and L/P decreased. We conclude that inspiratory loading is associated with an increase in the pulmonary transvascular hydrostatic gradient, possibly by causing a greater fall in interstitial perimicrovascular pressure than in microvascular pressure.

Relationship between weight gain and lymph flow in dog lungs

1983 ◽  
Vol 245 (1) ◽  
pp. H125-H130 ◽  
Author(s):  
R. E. Drake ◽  
R. L. Scott ◽  
J. C. Gabel
Keyword(s):  
Weight Gain ◽  
Lymph Flow ◽  
Base Line ◽  
Lung Weight ◽  
Lung Fluid ◽  
Lung Fluid Balance ◽  
Extravascular Volume ◽  
Continuous Weight ◽  
Lung Lymph ◽  
Lung Lymph Flow

Lung weight is a useful indicator of increases in lung extravascular volume. In addition, the lung lymph flow rate (QL) is an important factor in lung fluid balance. We have studied the weight and QL responses to elevations in capillary pressure (Pc) in intact dog lung lower left lobes. We measured lobe weight continuously. We also measured QL from small lymph vessels from the same lobes. The base-line QL was 1.7 +/- 1.5 microliter/min, and the weight was constant. After we increased Pc by 8-20 cmH2O, both weight and QL increased transiently. In most lungs the weight reached a new steady state. When we increased Pc further, weight increased continuously; however, QL reached a plateau. The continuous weight gain was due to edema. These results show that weight and QL respond similarly in nonedematous lungs; however, the weight and QL responses in edematous lungs may be different.

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