Increased pulmonary vascular permeability following acid aspiration

1981 ◽  
Vol 51 (2) ◽  
pp. 335-345 ◽  
Author(s):  
F. A. Grimbert ◽  
J. C. Parker ◽  
A. E. Taylor
Keyword(s):  
Intratracheal Instillation ◽  
Human Albumin ◽  
Lymph Flow ◽  
Lung Water ◽  
Fluid Filtration ◽  
Pulmonary Vascular Permeability ◽  
Acid Aspiration ◽  
Anesthetized Dogs ◽  
Lung Lymph ◽  
Lung Lymph Flow

The effect of hydrochloric acid aspiration on transvascular fluid and protein flux and lung water content was studied in 21 anesthetized dogs. We measured steady-state lung lymph flow, pulmonary arterial and left atrial pressures, and the concentration of total protein and albumin in both lymph and plasma after intratracheal instillation of 2 ml/kg 0.1 N HCl. Acid injury produced a twofold increase in lung lymph flow and lymph protein clearance when compared with control. This indicated an increase in pulmonary microvascular permeability. In dogs given 25 g concentrated human albumin and 1 mg/kg furosemide 10 min after the acid injury, the acid-induced increase in fluid filtration was prevented. However, the decrease in fluid filtration was not attributed to an increase in the transvascular protein osmotic pressure gradient but to a more direct effect of furosemide. Treatment with furosemide alone prevented the increase in lung lymph flow induced by acid injury, whereas albumin alone did not. In all acid-injured animals there was an increase in lung water when compared wtih control. Therefore acid aspiration produced localized areas of damage to filtration vessels that lead to increased leakage of protein and water. Furosemide treatment prevented much of this increased fluid and protein flux by an undefined mechanism.

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.

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)

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.

Effect of hypoxia on lung lymph flow in newborn lambs with left atrial hypertension

1988 ◽  
Vol 254 (3) ◽  
pp. H487-H493
Author(s):  
J. U. Raj ◽  
T. A. Hazinski ◽  
R. D. Bland
Keyword(s):  
Blood Flow ◽  
Left Atrial ◽  
Control Period ◽  
Lymph Flow ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Fluid Filtration ◽  
Alveolar Hypoxia ◽  
Lung Lymph ◽  
Lung Lymph Flow

To determine the effect of left atrial hypertension on the vascular response to hypoxia in the newborn lung, we measured pulmonary artery and left atrial pressures, lung blood flow and lymph flow, and concentrations of protein in lymph and plasma of 13 lambs that spontaneously breathed air for 2-6 h (control period), followed by 8-11% O2 mixed with 3-5% CO2 and N2 for 2-4 h (experimental period). In eight studies, the lambs were made hypoxic first, after which we elevated their left atrial pressure by 10-12 Torr for 2-3 h. In 10 additional studies, we reversed the sequence by raising left atrial pressure first followed by addition of hypoxia. In lambs with normal left atrial pressure, alveolar hypoxia increased both pulmonary blood flow and lymph flow, with an associated reduction in lymph-to-plasma protein ratio (L/P). When left atrial pressure was increased in the presence of hypoxia, lymph flow increased by a small amount and L/P decreased further. In lambs with preexisting left atrial pressure elevation, addition of alveolar hypoxia increased both blood flow and lymph flow with no significant change in L/P. These results suggest that in newborn lambs with normal left atrial pressure, alveolar hypoxia increases lung lymph flow mainly by increasing microvascular filtration pressure, whereas in lambs with elevated left atrial pressure, hypoxia increases lymph flow by another mechanism, perhaps by increasing the perfused surface area for fluid filtration.

Increasing duration of smoke exposure induces more severe lung injury in sheep

1988 ◽  
Vol 64 (3) ◽  
pp. 1107-1113 ◽  
Author(s):  
R. Kimura ◽  
L. D. Traber ◽  
D. N. Herndon ◽  
H. A. Linares ◽  
H. J. Lubbesmeyer ◽  
...  
Keyword(s):  
Lung Injury ◽  
Inhalation Injury ◽  
Lymph Flow ◽  
Smoke Inhalation ◽  
Lung Water ◽  
Arterial Blood ◽  
Chronic Study ◽  
Lung Lymph ◽  
Severe Lung ◽  
Lung Lymph Flow

Eighteen sheep previously prepared for chronic study were divided into three groups of six animals each. These were given graded inhalation injury utilizing smoke obtained from burning cotton-toweling material. Smoke was insufflated into animals with a modified bee smoker at temperatures less than 40 degrees C. Group H, which received 64 breaths of smoke, showed the most pronounced changes in pulmonary function. The changes consisted mainly of a profound increase in lung lymph flow following a reduced P/F ratio (PO2 in arterial blood/inspired O2 fraction) and an elevation in both thermal and gravimetrically measured extravascular lung water. Similar changes were seen in group M (48 breaths of smoke) and group L (32 breaths of smoke). However, the injury was graded based on the changes in gravimetrically measured lung water and lung lymph flow. These were highest in group H and lowest in group L. These studies confirm our ability to accurately quantitate the injury induced by smoke inhalation. In addition, it demonstrates that lung injury associated with the inhalation of smoke can be graded depending on the duration of exposure.

Role of sulfidopeptide leukotrienes in synthetic smoke inhalation injury in sheep

1990 ◽  
Vol 68 (5) ◽  
pp. 1962-1969 ◽  
Author(s):  
D. A. Quinn ◽  
D. Robinson ◽  
W. Jung ◽  
C. A. Hales
Keyword(s):  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Weight Ratio ◽  
Inhalation Injury ◽  
Lymph Flow ◽  
Smoke Inhalation ◽  
Lung Water ◽  
Smoke Inhalation Injury ◽  
Lung Lymph ◽  
Lung Lymph Flow

Acute lung injury with smoke inhalation results in significant morbidity and mortality. Previously we have shown that synthetic smoke composed of carbon and acrolein, a common component of smoke, causes delayed-onset noncardiogenic pulmonary edema. To study the possible role of the vasoactive and edemagenic sulfidopeptide leukotrienes (SPLT) in smoke inhalation injury, we measured pulmonary hemodynamics, lung lymph flow, and SPLT and leukotriene (LT) B4 in lung lymph before and after 10 min of synthetic acrolein smoke exposure. After smoke exposure there was a significant rise in pulmonary vascular resistance caused by a rise in pulmonary arterial pressure, a fall in cardiac output, and no change in pulmonary capillary wedge pressure. This was accompanied by an increase in total systemic vascular resistance (P less than 0.05), lung lymph flow (P less than 0.05), and extravascular lung water-to-lung dry weight ratio (P less than 0.05). Both SPLT and LTB4 clearance rose significantly (P less than 0.05), but there was a 10-fold increase in SPLT over LTB4 clearance. In sheep pretreated with FPL55712, a SPLT antagonist, the early rise in pulmonary vascular resistance was attenuated, and the rise in systemic vascular resistance was blocked. This was associated with an attenuated and delayed fall in cardiac output. FPL55712 had no effect on lung lymph flow or extravascular lung water-to-dry weight ratio. SPLT, and especially LTD4, may have a role in increased pulmonary and systemic vascular resistance after smoke inhalation injury but does not appear to affect vascular permeability.

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.

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