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.

Effects of left atrial pressure on the pulmonary vascular response to hypoxic ventilation

1991 ◽  
Vol 70 (5) ◽  
pp. 1991-1995 ◽  
Author(s):  
S. A. Gu ◽  
J. Ducas ◽  
U. Schick ◽  
R. M. Prewitt
Keyword(s):  
Arterial Pressure ◽  
Left Atrial ◽  
Pulmonary Arterial Pressure ◽  
Mean Value ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Vascular Response ◽  
Wide Range ◽  
Pulmonary Arterial ◽  
The Mean

We investigated the effects of hypoxic ventilation on the pulmonary arterial pressure- (P) flow (Q) relationship in an intact canine preparation. Mean pulmonary P-Q coordinates were obtained during hypoxic ventilation and during ventilation with 100% O2 at normal and at increased left atrial pressure. Specifically, we tested the hypothesis that, over a wide range, changes in left atrial pressure would alter the effects of hypoxic ventilation on pulmonary P-Q characteristics. Seven dogs were studied. When left atrial pressure was normal (5 mmHg), the mean value of the extrapolated intercept (PI) of the linear P-Q relationship was 10.9 mmHg and the slope (incremental vascular resistance, IR) of the P-Q relationship was 2.2 mmHg.l-1.min. Hypoxic ventilation increased PI to 18 mmHg (P less than 0.01) but did not affect IR. Subsequently, during ventilation with 100% O2, when left atrial pressure was increased to 14 mmHg by inflation of left atrial balloon, PI increased to 18 mmHg. IR was 1.6 mmHg.l-1.min. Again, hypoxic ventilation caused an isolated change in PI. Hypoxia increased PI from 18 to 28 mmHg (P less than 0.01). As in the condition of normal left atrial pressure, hypoxic ventilation did not affect IR. We conclude that, in an anesthetized intact canine preparation, hypoxic ventilation causes an isolated increase in the extrapolated pressure intercept of the pulmonary P-Q relationship. Furthermore the effects of hypoxic ventilation on pulmonary P-Q characteristics are not affected by the resting left atrial pressure.

Air embolism-induced lung injury in isolated rat lungs

1992 ◽  
Vol 72 (4) ◽  
pp. 1235-1242 ◽  
Author(s):  
D. Wang ◽  
M. H. Li ◽  
K. Hsu ◽  
C. Y. Shen ◽  
H. I. Chen ◽  
...  
Keyword(s):  
Weight Gain ◽  
Lung Injury ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Air Embolism ◽  
Lavage Fluid ◽  
Lung Lavage ◽  
Lung Model ◽  
Lung Weight ◽  
Pulmonary Arterial

Pulmonary air embolism causes physical obstruction of microvasculature and leads to permeability changes, release of mediators, and injury to lung tissue. In this study we employed an isolated perfused rat lung model to investigate the primary and secondary effects produced by infusion of air into the pulmonary artery. Infusion of various doses of air (0.10–0.25 ml) over a 1-min period produced a dose-dependent increase in pulmonary arterial pressure and lung weight gain. In contrast, when a constant air dose was administered over various periods of time (0.25 ml over 0.5–8.0 min), the pulmonary arterial pressure rose to the same extent regardless of the infusion rate, whereas the lung weight gain increased proportionately with the rate of infusion. Total vascular resistance rose from 1.41 +/- 0.04 to 5.04 +/- 0.09 mmHg.ml-1.min in rats given 0.25 ml air over 1 min (n = 14, P less than 0.001), with greater than or equal to 90% of this increase occurring in the arterial segments. Both thromboxane B2 and endothelin concentrations also increased in the perfusate, suggesting their involvement in this increased resistance. Furthermore the pulmonary filtration coefficient increased from 0.21 +/- 0.05 to 1.28 +/- 0.26 g.min-1.cmH2O–1.100 g (n = 8, P less than 0.001), and the protein concentration in lung lavage fluid also rose, indicating lung injury. Leukocyte counts in the perfusate were unaffected by embolization, but chemiluminescent activity was increased, indicating a possible role for activated leukocytes in lung injury induced by air emboli.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

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)

Chronic lung lymph fistula that only drains the left lung

1995 ◽  
Vol 269 (4) ◽  
pp. R943-R947
Author(s):  
Y. Kikuchi ◽  
H. Nakazawa ◽  
D. L. Traber
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Mediastinal Lymph Node ◽  
Pulmonary Veins ◽  
Pulmonary Arteries ◽  
Left Lung ◽  
Lymph Flow ◽  
Pulmonary Arterial ◽  
The Right ◽  
Arteries And Veins

We developed a chronic lung fistula that drains only the left lung, allowing for evaluation of injury in a single lung. To remove lymph drainage from the right lung into the caudal mediastinal lymph node, the right lower pulmonary ligament was severed. Pneumatic occluders were placed on the left pulmonary arteries and veins. To ensure that lymph drained from only the left lung, we increased the right pulmonary arterial pressure (RPAP) from 21.2 +/- 0.5 to 36.5 +/- 0.6 mmHg. The left pulmonary arterial pressure (LPAP) was kept at wedge pressure level for 1 h by inflating pneumatic occluders. Lymph flow from the left lung fistula was stable during this occlusion. Six hours after recovery was increased the LPAP from a baseline level of 19.1 +/- 1.0 to 36.4 +/- 0.9 mmHg and the RPAP from 21.2 +/- 0.5 to 38.0 +/- 0.8 mmHg for 2 h by inflating the pneumatic occluders on the left and right pulmonary veins. Lymph flow increased from 5.3 +/- 1.0 to 28.0 +/- 2.9 ml/h. Reflection coefficient was calculated at 0.80 +/- 0.02.

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)

Cyclooxygenase and lipoxygenase inhibition by BW-755C reduces acrolein smoke-induced acute lung injury

1994 ◽  
Vol 77 (2) ◽  
pp. 888-895 ◽  
Author(s):  
S. P. Janssens ◽  
S. W. Musto ◽  
W. G. Hutchison ◽  
C. Spence ◽  
M. Witten ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Arterial Pressure ◽  
Pulmonary Edema ◽  
Pulmonary Arterial Pressure ◽  
Weight Ratio ◽  
Peak Inspiratory Pressure ◽  
Dry Weight ◽  
Lymph Flow ◽  
Pulmonary Arterial ◽  
Arterial Po2

Inhalation of smoke containing acrolein, the most common toxin in urban fires after carbon monoxide, causes vascular injury with non-cardiogenic pulmonary edema containing potentially edematogenic eicosanoids such as thromboxane (Tx) B2, leukotriene (LT) B4, and the sulfidopeptide LTs (LTC4, LTD4, and LTE4). To determine which eicosanoids are important in the acute lung injury, we pretreated sheep with BW-755C (a combined cyclooxygenase and lipoxygenase inhibitor), U-63557A (a specific Tx synthetase inhibitor), or indomethacin (a cyclooxygenase inhibitor) before a 10-min exposure to a synthetic smoke containing carbon particles (4 microns) with acrolein and compared the results with those from control sheep that received only carbon smoke. Acrolein smoke induced a fall in arterial PO2 and rises in peak inspiratory pressure, main pulmonary arterial pressure, pulmonary vascular resistance, lung lymph flow, and the blood-free wet-to-dry weight ratio. BW-755C delayed the rise in peak inspiratory pressure and prevented the fall in arterial PO2, the rise in lymph flow, and the rise in wet-to-dry weight ratio. Neither indomethacin nor U-63557A prevented the increase in lymph flow or wet-to-dry weight ratio, although they did blunt and delay the rise in airway pressure and did prevent the rises in pulmonary arterial pressure and pulmonary vascular resistance. Thus, cyclooxygenase products, probably Tx, are responsible for the pulmonary hypertension after acrolein smoke and to some extent for the increased airway resistance but not the pulmonary edema. Prevention of high-permeability pulmonary edema after smoke with BW-755C suggests that LTB4, may be etiologic, as previous work has eliminated LTC4, LTD4, and LTE4.

Effect of thoracic duct drainage on hydrostatic pulmonary edema and pleural effusion in sheep

1991 ◽  
Vol 71 (1) ◽  
pp. 314-316 ◽  
Author(s):  
S. J. Allen ◽  
R. E. Drake ◽  
G. A. Laine ◽  
J. C. Gabel
Keyword(s):  
Pleural Effusion ◽  
Central Venous Pressure ◽  
Pulmonary Edema ◽  
Thoracic Duct ◽  
Left Atrial ◽  
Venous Pressure ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Central Venous ◽  
Pulmonary Arterial

Positive end-expiratory pressure (PEEP) increases central venous pressure, which in turn impedes return of systemic and pulmonary lymph, thereby favoring formation of pulmonary edema with increased microvascular pressure. In these experiments we examined the effect of thoracic duct drainage on pulmonary edema and hydrothorax associated with PEEP and increased left atrial pressure in unanesthetized sheep. The sheep were connected via a tracheostomy to a ventilator that supplied 20 Torr PEEP. By inflation of a previously inserted intracardiac balloon, left atrial pressure was increased to 35 mmHg for 3 h. Pulmonary arterial, systemic arterial, and central venous pressure as well as thoracic duct lymph flow rate were continuously monitored, and the findings were compared with those in sheep without thoracic duct cannulation (controls). At the end of the experiment we determined the severity of pulmonary edema and the volume of pleural effusion. With PEEP and left atrial balloon insufflation, central venous and pulmonary arterial pressure were increased approximately threefold (P less than 0.05). In sheep with a thoracic duct fistula, pulmonary edema was less (extra-vascular fluid-to-blood-free dry weight ratio 4.8 +/- 1.0 vs. 6.1 +/- 1.0; P less than 0.05), and the volume of pleural effusion was reduced (2.0 +/- 2.9 vs. 11.3 +/- 9.6 ml; P less than 0.05). Our data signify that, in the presence of increased pulmonary microvascular pressure and PEEP, thoracic duct drainage reduces pulmonary edema and hydrothorax.

Effects of transient pulmonary hypertension on pulmonary vascular permeability

1983 ◽  
Vol 55 (3) ◽  
pp. 983-989 ◽  
Author(s):  
F. L. Minnear ◽  
P. S. Barie ◽  
A. B. Malik
Keyword(s):  
Pulmonary Edema ◽  
Vascular Permeability ◽  
Left Atrial ◽  
Lymph Flow ◽  
Balloon Inflation ◽  
Lung Water ◽  
Lung Weight ◽  
Pulmonary Vascular Permeability ◽  
Airway Edema ◽  
Vascular Surface

The effects of a transient increase in pulmonary microvascular pressure (Pmv) on pulmonary fluid and protein exchange were studied in anesthetized sheep in which pulmonary lymph was collected. Pmv was increased to 30-40 mmHg for 15-30 min in 18 sheep by either an intra-aortic injection of norepinephrine (NE) or a rapid inflation of a left atrial balloon. NE injection produced sustained two- to threefold increases in pulmonary lymph flow and protein flux, whereas rapid balloon inflation transiently elevated lymph flow even though Pmv increased to similar levels with both methods. The sustained increases with NE were not due to an increase in vascular permeability but probably the result of a persistent increase in vascular surface area. In three additional animals, Pmv was increased to over 50 mmHg for 15-30 min. In these animals, lymph flow increased only by 49%, but airway edema fluid was present. The ratio of extravascular lung water to bloodless dry lung weight was 5.77 +/- 0.13 as compared with 4.30 +/- 0.11 in sheep subjected to Pmv less than 50 mmHg and to 4.08 +/- 0.19 for controls. These findings indicate that high pressure-induced pulmonary edema depends on a threshold Pmv around 50 mmHg. A combination of high capillary pressure and impaired lymphatic flow may be the bases for the development of neurogenic and catecholamine-induced pulmonary edema.

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