Effect of regional alveolar hypoxia on permeability pulmonary edema formation in dogs

1987 ◽  
Vol 62 (4) ◽  
pp. 1690-1697 ◽  
Author(s):  
F. W. Cheney ◽  
M. J. Bishop ◽  
E. Y. Chi ◽  
B. L. Eisenstein
Keyword(s):  
Pulmonary Edema ◽  
Lower Lobe ◽  
Dry Weight ◽  
Left Pulmonary Artery ◽  
Edema Formation ◽  
Pulmonary Capillary ◽  
Anesthetized Dogs ◽  
Alveolar Hypoxia ◽  
Permeability Pulmonary Edema ◽  
The Right

We studied the effects of regional alveolar hypoxia on permeability pulmonary edema formation. Anesthetized dogs had a bronchial divider placed so that the left lower lobe (LLL) could be ventilated with a hypoxic gas mixture (HGM) while the right lung was continuously ventilated with 100% O2. Bilateral permeability edema was induced with 0.05 ml/kg oleic acid and after 4 h of LLL ventilation with an HGM (n = 9) LLL gross weight was 161 +/- 13 (SE) g compared with 204 +/- 13 (SE) g (P less than 0.05) in the right lower lobe (RLL). Bloodless lobar water and dry weight were also significantly lower in the LLL as compared with the RLL of the study animals. In seven control animals in which the LLL fractional inspired concentration of O2 (FIO2) was 1.0 during permeability edema, there were no differences in gravimetric variables between LLL and RLL. In eight additional animals, pulmonary capillary pressure (Pc), measured by simultaneous occlusion of left pulmonary artery and vein, was not significantly different between LLL FIO2 of 1.0 and 0.05 either before or after pulmonary edema. We conclude that, in the presence of permeability pulmonary edema, regional alveolar hypoxia causes reduction in edema formation. The decreased edema formation during alveolar hypoxia is not due to a reduction in Pc.

Lack of alveolar O2 during lung reperfusion does not decrease edema formation

1989 ◽  
Vol 67 (2) ◽  
pp. 528-533 ◽  
Author(s):  
P. T. Overand ◽  
M. J. Bishop ◽  
B. L. Eisenstein ◽  
E. Y. Chi ◽  
M. Su ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Left Lung ◽  
Lower Lobe ◽  
Arterial Occlusion ◽  
Dry Weight ◽  
Left Pulmonary Artery ◽  
Left Lower Lobe ◽  
Edema Formation ◽  
Alveolar Hypoxia ◽  
The Right

We previously reported that pulmonary arterial occlusion for 48 h followed by 4 h of reperfusion in awake dogs results in marked edema and inflammatory infiltrates in both reperfused and contralateral lungs (Am. Rev. Respir. Dis. 134: 752–756, 1986; J. Appl. Physiol. 63: 942–950, 1987). In this experiment we study the effects of alveolar hypoxia on this injury. Anesthetized dogs underwent thoracotomy and occlusion of the left pulmonary artery. Twenty-four hours later the dogs were reanesthetized, and a double-lumen endotracheal tube was placed. The right lung was continuously ventilated with an inspiratory O2 fraction (FIO2) of 0.35. In seven study animals the left lung was ventilated with an FIO2 of 0 for 3 h after the left pulmonary artery occluder was removed. In six control animals the left lung was ventilated with an FIO2 of 0.35 during the same reperfusion period. Postmortem bloodless wet-to-dry weight ratios were 5.87 +/- 0.20 for the left lower lobe and 5.32 +/- 0.12 for the right lower lobe in the dogs with hypoxic ventilation (P less than 0.05 for right vs. left lobes). These values were not significantly different from the control dog lung values of 5.94 +/- 0.22 for the left lower lobe and 5.11 +/- 0.07 for the right lower lobe (P less than 0.05 for right vs. left lobes). All values were significantly higher than our laboratory normal of 4.71 +/- 0.06. We conclude that reperfusion injury is unaffected by alveolar hypoxia during the reperfusion phase.

Regional alveolar hypoxia does not affect air embolism-induced pulmonary edema

1989 ◽  
Vol 66 (5) ◽  
pp. 2369-2373 ◽  
Author(s):  
F. W. Cheney ◽  
B. L. Eisenstein ◽  
P. T. Overand ◽  
M. J. Bishop
Keyword(s):  
Pulmonary Edema ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Femoral Vein ◽  
Lower Lobe ◽  
Air Embolism ◽  
Dry Weight ◽  
Double Lumen Tube ◽  
Edema Formation ◽  
Alveolar Hypoxia ◽  
Permeability Pulmonary Edema

We studied the effects of regional alveolar hypoxia on permeability pulmonary edema resulting from venous air embolization. Anesthetized dogs had the left upper lobe removed and a double-lumen tube placed so that right lung and left lower lobe (LLL) could be ventilated independently. Air was infused into the femoral vein for 1 h during bilateral ventilation at an inspiratory O2 fraction (FIO2) of 1.0. After cessation of air infusion the LLL was then ventilated with a hypoxic gas mixture (FIO2 = 0.05) in six animals and an FIO2 of 1.0 in six other animals. Lung hydroxyproline content was measured as an index of lung dry weight. LLL bloodless lobar wet weight-to-hydroxyproline ratio was 0.33 +/- 0.06 mg/micrograms in the animals exposed to LLL hypoxia and 0.37 +/- 0.03 mg/micrograms (NS) in the animals that had a LLL FIO2 of 1. Both values were significantly higher than our laboratory normal values of 0.19 +/- 0.01 mg/micrograms. We subsequently found in four more dogs exposed to global alveolar hypoxia before and after air embolism that the air injury itself significantly depressed the hypoxic vasoconstrictor response. We conclude that regional alveolar hypoxia has no effect on pulmonary edema formation due to air embolism. The most likely reason for these findings is that the air embolism injury itself interfered with hypoxic pulmonary vasoconstriction.

Effect of regional alveolar hypoxia on gas exchange in dogs

1989 ◽  
Vol 67 (2) ◽  
pp. 730-735 ◽  
Author(s):  
K. B. Domino ◽  
M. P. Hlastala ◽  
B. L. Eisenstein ◽  
F. W. Cheney
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Lower Lobe ◽  
Dispersion Index ◽  
Anesthetized Dogs ◽  
Alveolar Hypoxia ◽  
The Right ◽  
Increased Blood Flow ◽  
Hypoxic Gas Mixture ◽  
Hypoxic Region

We studied the effects of left lower lobe (LLL) alveolar hypoxia on pulmonary gas exchange in anesthetized dogs using the multiple inert gas elimination technique (MIGET). The left upper lobe was removed, and a bronchial divider was placed. The right lung (RL) was continuously ventilated with 100% O2, and the LLL was ventilated with either 100% O2 (hyperoxia) or a hypoxic gas mixture (hypoxia). Whole lung and individual LLL and RL ventilation-perfusion (VA/Q) distributions were determined. LLL hypoxia reduced LLL blood flow and increased the perfusion-related indexes of VA/Q heterogeneity, such as the log standard deviation of the perfusion distribution (log SDQ), the retention component of the arterial-alveolar difference area [R(a-A)D], and the retention dispersion index (DISPR*) of the LLL. LLL hypoxia increased blood flow to the RL and reduced the VA/Q heterogeneity of the RL, indicated by significant reductions in log SDQ, R(a-A)D, and DISPR*. In contrast, LLL hypoxia had little effect on gas exchange of the lung when evaluated as a whole. We conclude that flow diversion induced by regional alveolar hypoxia preserves matching of ventilation to perfusion in the whole lung by increasing gas exchange heterogeneity of the hypoxic region and reducing heterogeneity in the normoxic lung.

PEEP is necessary for exogenous surfactant to reduce pulmonary edema in canine aspiration pneumonitis

1992 ◽  
Vol 73 (2) ◽  
pp. 679-686 ◽  
Author(s):  
A. R. Zucker ◽  
B. A. Holm ◽  
G. P. Crawford ◽  
K. Ridge ◽  
L. D. Wood ◽  
...  
Keyword(s):  
Lung Injury ◽  
Lung Surfactant ◽  
Dry Weight ◽  
Exogenous Surfactant ◽  
Edema Formation ◽  
A Value ◽  
Pulmonary Capillary ◽  
Injury Model ◽  
Lung Injury Model ◽  
Anesthetized Dogs

Alveolar edema inactivates surfactant, and surfactant depletion causes edema by reducing lung interstitial pressure (Pis). We reasoned that surfactant repletion might reduce edema by raising Pis after acute lung injury and that positive end-expiratory pressure (PEEP) might facilitate this effect. One hour after tracheal administration of hydrochloric acid in 18 anesthetized dogs with transmural pulmonary capillary wedge pressure of 8 Torr, the animals were randomized into three groups: in the SURF + PEEP group, 50 mg/kg of calf lung surfactant extract (CLSE) was instilled into each main stem bronchus with 8 cmH2O of PEEP; in the SAL + PEEP group, PEEP was followed by an equal volume of saline (SAL); in the SURF group, CLSE was given without PEEP. After 5 h, edema in excised lungs (wet-to-dry weight ratios) was significantly less in the SURF + PEEP group (9.1 +/- 1.0) than in the other groups (11.3 +/- 1.8 and 11.3 +/- 1.8, respectively). In the SURF + PEEP group, pulmonary venous admixture fell by 6%; this change was different from the 7% increase in the SAL + PEEP group and 40% increase in the SURF group (P less than 0.05). Airway secretions obtained in the SURF + PEEP group had normal minimum surface tensions of 4 +/- 2 mN/m, a value much lower than in SAL + PEEP and SURF groups (32 +/- 4 and 22 +/- 7 mN/m, respectively). We conclude that surfactant normalizes surface tension and decreases transcapillary hydrostatic forces in this lung injury model, thereby reducing edema formation and improving gas exchange. These benefits occur only if surfactant is given with PEEP, allowing surfactant access to the alveoli and/or minimizing its inhibition by edema proteins.

Hyperthermia-induced pulmonary edema

1986 ◽  
Vol 60 (6) ◽  
pp. 1980-1985 ◽  
Author(s):  
K. Y. Mustafa ◽  
W. M. Selig ◽  
K. E. Burhop ◽  
F. L. Minnear ◽  
A. B. Malik
Keyword(s):  
Pulmonary Edema ◽  
Capillary Pressure ◽  
Dry Weight ◽  
Base Line ◽  
Lung Weight ◽  
Edema Formation ◽  
Control Value ◽  
Pulmonary Capillary ◽  
Pulmonary Capillary Pressure ◽  
Isolated Lungs

The effects of temperature (37–45 degrees C) on pulmonary edema formation and transendothelial albumin clearance were investigated using isolated perfused guinea pig lungs and bovine pulmonary arterial endothelial cells grown to confluency on a gelatinized membrane. Perfusion of isolated lungs with Ringer-albumin solution at 37 or 41 degrees C for 90 min produced no change in lung wet-to-dry weight ratios (W/D) or in pulmonary capillary pressure (measured by the double-occlusion method). When perfused at 43 degrees C, lung wet weight increased 0.8 +/- 0.4 g over base line (final W/D = 7.43 +/- 0.7) within 90 min. Perfusion at 45 degrees C increased lung weight by 2.7 +/- 0.9 g over base line (final W/D 11.8 +/- 2.3 vs. control value of 5.2 +/- 0.23 at 37 degrees C perfusion) within 60 min. The changes in pulmonary capillary pressure were small (from a base-line value of 4.3 +/- 0.8 to 4.9 +/- 0.4 at 43 degrees C and from a base-line value of 4.9 +/- 0.8 to 5.9 +/- 0.6 at 45 degrees C). The clearance of 125I-albumin (microliter/min) across the endothelial monolayer system increased threefold (from 0.295 +/- 0.035 to 1.048 +/- 0.107) at 45 degrees C, an effect comparable to positive controls of trypsin (from 0.272 +/- 0.046 to 1.595 +/- 0.138) or oleic acid (from 0.278 +/- 0.043 to 0.672 +/- 0.26). An increase in temperature from 37 to 45 degrees C had no effect on the permeability of the gelatinized membrane alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary blood flow and ventilation-perfusion heterogeneity

1991 ◽  
Vol 71 (1) ◽  
pp. 252-258 ◽  
Author(s):  
K. B. Domino ◽  
B. L. Eisenstein ◽  
F. W. Cheney ◽  
M. P. Hlastala
Keyword(s):  
Blood Flow ◽  
Standard Deviation ◽  
Gas Exchange ◽  
Minute Ventilation ◽  
Lower Lobe ◽  
Left Pulmonary Artery ◽  
Pulmonary Gas Exchange ◽  
Ventilation Distribution ◽  
Anesthetized Dogs ◽  
The Right

We studied the independent influence of changes in perfusion on pulmonary gas exchange in the left lower lobe (LLL) of anesthetized dogs. Blood flow to the LLL (QLLL) was raised 50% (increased QLLL) or reduced 50% (decreased QLLL) from baseline by partial occlusion of the right or left pulmonary artery, respectively. Minute ventilation and alveolar PCO2 of the LLL remained constant throughout the study. We determined ventilation-perfusion distributions of the LLL using the multiple inert gas elimination technique. Increased QLLL impaired LLL pulmonary gas exchange. All dispersion indexes and all arterial-alveolar difference areas increased (P less than 0.01). Decreased QLLL increased the log standard deviation of the perfusion distribution (P less than 0.05) and reduced the log standard deviation of the ventilation distribution (P less than 0.01) but did not affect the dispersion indexes or alveolar-arterial difference areas. We conclude that ventilation-perfusion heterogeneity is increased by independent changes in perfusion from normal baseline blood flow, even when ventilation and alveolar gas composition remain constant.

Effect of pulmonary artery occlusion and reperfusion on extravascular fluid accumulation

1981 ◽  
Vol 50 (1) ◽  
pp. 102-106 ◽  
Author(s):  
P. S. Barie ◽  
T. S. Hakim ◽  
A. B. Malik
Keyword(s):  
Pulmonary Artery ◽  
Water Content ◽  
Left Atrial ◽  
Left Lung ◽  
Weight Ratio ◽  
Dry Weight ◽  
Left Pulmonary Artery ◽  
Artery Occlusion ◽  
Lung Water ◽  
The Right

We determined the effect of pulmonary hypoperfusion on extravascular water accumulation in anesthetized dogs by occluding the left pulmonary artery for 3 h and then reperfusing it for 24 h. The lung was reperfused either at normal left atrial pressure (Pla) or during increased Pla induced by a left atrial balloon. In each case the extravascular water content-to-bloodless dry weight ratio (W/D) of the left lung was compared with that of the right lung. The W/D of the left lung of 3.26 +/- 0.49 ml/g was not significantly different from the value of 2.87 +/- 0.37 for the right lung after the reperfusion at normal Pla. However, the W/D of the left lung of 5.10 +/- 0.38 ml/g was greater (P less than 0.05) than the value of 4.42 +/- 0.34 for the right lung after reperfusion at Pla of 25 Torr. This difference could not be prevented by pretreatment with heparin, suggesting that the increase in lung water content was not due to activation of intravascular coagulation secondary to stasis occurring during the occlusion. Because the left lung was more edematous than the right one, even though both lungs had been subjected to the same increase in Pla, the results suggest that a period of pulmonary hypoperfusion causes an increase in the interstitial protein concentration.

Edema from cyclooxygenase products of endogenous arachidonic acid in isolated lung

1989 ◽  
Vol 67 (2) ◽  
pp. 846-855 ◽  
Author(s):  
M. R. Littner ◽  
F. D. Lott
Keyword(s):  
Arachidonic Acid ◽  
Pulmonary Edema ◽  
Enzyme Inhibitor ◽  
Calcium Ionophore ◽  
Dry Weight ◽  
Lung Water ◽  
Isolated Lung ◽  
Pulmonary Arterial ◽  
Area Product ◽  
Permeability Pulmonary Edema

We infused A23187, a calcium ionophore, into the pulmonary circulation of dextran-salt-perfused isolated rabbit lungs to release endogenous arachidonic acid. This led to elevations in pulmonary arterial pressure and to pulmonary edema as measured by extravascular wet-to-dry weight ratios. The increase in pressure and edema was prevented by indomethacin, a cyclooxygenase enzyme inhibitor, and by 1-benzylimidazole, a selective inhibitor of thromboxane (Tx) A2 synthesis. Transvascular flux of 125I-albumin from vascular to extravascular spaces of the lung was not elevated by A23187 but was elevated by infusion of oleic acid, an agent known to produce permeability pulmonary edema. We confirmed that A23187 leads to elevations in cyclooxygenase products and that indomethacin and 1-benzylimidazole inhibit synthesis of all cyclooxygenase products and TxA2, respectively, by measuring perfusate levels of prostaglandin (PG) I2 as 6-ketoprostaglandin F1 alpha, PGE2, and PGF2 alpha and TxA2 as TxB2. We conclude that release of endogenous pulmonary arachidonic acid can lead to pulmonary edema from conversion of such arachidonic acid to cyclooxygenase products, most notably TxA2. This edema was most likely from a net hydrostatic accumulation of extravascular lung water with an unchanged permeability of the vascular space, since an index of permeability-surface area product (i.e., transvascular albumin flux) was not increased.

Lipoxygenase and cyclooxygenase blockade by BW 755C enhances pulmonary hypoxic vasoconstriction

1987 ◽  
Vol 62 (1) ◽  
pp. 129-133 ◽  
Author(s):  
R. C. Garrett ◽  
S. Foster ◽  
H. M. Thomas
Keyword(s):  
Sulfur Hexafluoride ◽  
Pressor Response ◽  
Lower Lobe ◽  
Shunt Fraction ◽  
Lipoxygenase Pathway ◽  
Hypoxic Vasoconstriction ◽  
Anesthetized Dogs ◽  
Receptor Blockers ◽  
Alveolar Hypoxia ◽  
Leukotriene Receptor

Lipoxygenase products (leukotrienes) have been proposed as the mediators of pulmonary hypoxic vasoconstriction. However, the supporting data are inconclusive because the lipoxygenase and leukotriene receptor blockers that reduce hypoxic vasoconstriction (such as diethylcarbamazine and the FPL's) have confounding effects. We investigated BW 755C, a potent inhibitor of both lipoxygenase and cyclooxygenase, in eight intact anesthetized dogs with acute left lower lobe atelectasis. We examined two manifestations of hypoxic vasoconstriction: shunt fraction, as an inverse indicator of regional constriction in response to local hypoxia, and the pulmonary pressor response to global alveolar hypoxia, as an index of general hypoxic vasoconstriction. During normoxia, shunt fraction, measured using a sulfur hexafluoride infusion, was 32.0 +/- 7.0%. The pulmonary pressor response to hypoxia, defined as the increase in pulmonary end-diastolic gradient produced by 10% O2 inhalation, averaged 4.5 +/- 1.8 mmHg. Then, during normoxia, BW 755C was administered. Shunt fraction fell in all eight dogs from the previous mean of 32% to 25.5 +/- 6.1% (t = 6.5, P less than 0.0005). The hypoxic pressor response rose in all dogs, from the previous 4.5 mmHg to 9.0 +/- 3.5 mmHg (t = 4.5, P less than 0.005). BW 755C enhances hypoxic vasoconstriction, an effect consistent with its activity as a cyclooxygenase inhibitor. These data do not support a substantive role for the lipoxygenase pathway in hypoxic vasoconstriction.

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