Microvascular injury distal to unilateral pulmonary artery occlusion

1981 ◽  
Vol 51 (4) ◽  
pp. 845-851 ◽  
Author(s):  
R. L. Johnson ◽  
S. S. Cassidy ◽  
M. Haynes ◽  
R. L. Reynolds ◽  
W. Schulz

We explored three questions: 1) does edema fluid accumulate distal to temporary unilateral pulmonary artery occlusion (TUPAO); 2) if so how rapidly does it accumulate; and 3) how is it affected by positive end-expiratory pressure (PEEP)? Using a tracheal divider we measured pulmonary capillary blood flow (Qc), tissue volume (Vt), and diffusing capacity (DLCO) in each lung with a rebreathing method. After control measurements in 12 dogs, the left pulmonary artery was occluded and measurements were repeated at intervals during 4 h of occlusion and 30 min after release of the occlusion. Six of the dogs were ventilated with 10 cmH2O PEEP. Finally the lungs were removed, weighed, and fixed for histology. TUPAO caused a 29% increase in Vt of the left lung without PEEP and a 59% increase with PEEP. After release of the occlusion, Qc and DLCO in the left lung returned to control levels within 30 min in dogs not on PEEP but remained depressed in dogs ventilated with PEEP even though PEEP was removed. At postmortem the left lung weighed more than expected in both groups of dogs but was significantly heavier in those on PEEP. Histology confirmed bronchovascular cuffing with edema and hemorrhage.

1981 ◽  
Vol 50 (1) ◽  
pp. 102-106 ◽  
Author(s):  
P. S. Barie ◽  
T. S. Hakim ◽  
A. B. Malik

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.


1965 ◽  
Vol 20 (1) ◽  
pp. 79-86 ◽  
Author(s):  
E. M. Cree ◽  
H. K. Rasmussen ◽  
F. Wright ◽  
J. K. Curtis

Bilateral bronchospirometric nitrogen washout studies were used for the first time to calculate ventilation/perfusion ratios for the well and poorly ventilated areas in individual lungs. Results were compared with washout studies on both lungs measured together. Data suitable for analysis were obtained from seven patients with chronic lung disease. It was demonstrated that this technique for determining simultaneous ventilation/perfusion ratios for each lung gave accurate and detailed physiological changes. Comparison of the sum of average values for pulmonary capillary blood flow when both lungs were measured together by the same nitrogen washout technique showed a variation within the accepted 10% error for cardiac output. Diffusion for the separate lungs, measured by the carbon monoxide breath-holding method, gave values which correlated with lung volumes. bronchospirometry; nitrogen washout; diffusing capacity Submitted on November 22, 1963


1965 ◽  
Vol 44 (10) ◽  
pp. 1591-1599 ◽  
Author(s):  
J R Nairn ◽  
G G Power ◽  
R W Hyde ◽  
R E Forster ◽  
C J Lambertsen ◽  
...  

1985 ◽  
Vol 68 (s11) ◽  
pp. 6P-6P
Author(s):  
D.F. Treacher ◽  
T.K. Cowell ◽  
N.T. Bateman ◽  
I.R. Cameron ◽  
R.D. Bradley

2003 ◽  
Vol 95 (1) ◽  
pp. 3-10 ◽  
Author(s):  
M. Rohdin ◽  
J. Petersson ◽  
P. Sundblad ◽  
M. Mure ◽  
R. W. Glenny ◽  
...  

Both in normal subjects exposed to hypergravity and in patients with acute respiratory distress syndrome, there are increased hydrostatic pressure gradients down the lung. Also, both conditions show an impaired arterial oxygenation, which is less severe in the prone than in the supine posture. The aim of this study was to use hypergravity to further investigate the mechanisms behind the differences in arterial oxygenation between the prone and the supine posture. Ten healthy subjects were studied in a human centrifuge while exposed to 1 and 5 times normal gravity (1 G, 5 G) in the anterioposterior (supine) and posterioanterior (prone) direction. They performed one rebreathing maneuver after ∼5 min at each G level and posture. Lung diffusing capacity decreased in hypergravity compared with 1 G (ANOVA, P = 0.002); it decreased by 46% in the supine posture compared with 25% in the prone ( P = 0.01 for supine vs. prone). At the same time, functional residual capacity decreased by 33 and 23%, respectively ( P < 0.001 for supine vs. prone), and cardiac output by 40 and 31% ( P = 0.007 for supine vs. prone), despite an increase in heart rate of 16 and 28% ( P < 0.001 for supine vs. prone), respectively. The finding of a more impaired diffusing capacity in the supine posture compared with the prone at 5 G supports our previous observations of more severe arterial hypoxemia in the supine posture during hypergravity. A reduced pulmonary-capillary blood flow and a reduced estimated alveolar volume can explain most of the reduction in diffusing capacity when supine.


1985 ◽  
Vol 69 (3) ◽  
pp. 279-286 ◽  
Author(s):  
Françloise Dargent ◽  
Jean-Patrice Gardaz ◽  
Philippe Morel ◽  
Peter M. Suter ◽  
Alain F. Junod

1. To test the relative sensitivity of serotonin and propranolol pulmonary extraction measurements to changes in pulmonary vascular surface, we sequentially subjected anaesthetized dogs to left upper lobe atelectasis, left lung atelectasis and left pulmonary artery occlusion. 2. We used a triple-indicator dilution technique to simultaneously measure the pulmonary extraction of serotonin and propranolol. After an initial series of measurements, dogs received dopamine and dextran to slightly increase pulmonary artery pressure and prevent further recruitment of capillaries. 3. Left upper lobe atelectasis did not modify the pulmonary extraction of serotonin and propranolol. Left lung atelectasis provoked a reduction in the serotonin extraction ratio by only 4%, whereas the propranolol extraction ratio decreased by 13%. After left pulmonary artery occlusion, propranolol and serotonin extraction ratios decreased by 16% and 5% respectively. 4. We conclude that the pulmonary extraction of propranolol is more sensitive to a decrease in pulmonary vascular surface than that of serotonin.


1980 ◽  
Vol 3 (5) ◽  
pp. 259-262 ◽  
Author(s):  
J.T. Morrison ◽  
A.F. Wilson ◽  
N.D. Vaziri ◽  
L. Brunsting ◽  
J. Davis

In order to better understand changes in lung function before and after dialysis, we studied eight patients with end-stage renal disease undergoing chronic hemodialysis. Pulmonary tissue volume (Vt), pulmonary capillary blood flow (Q̇c), the diffusing capacity for carbon monoxide (DLCO), arterial blood gases and body weight were measured before and after dialysis. A single breath, constant expiratory flow technique for determination of DLCO, Q̇c and Vt was used. DLCO, Q̇c, arterial carbon dioxide, and body weight were reduced post dialysis (P ≤ .01) while Vt failed to change. The alveolar-arterial oxygen difference rose 12 mmHg (P = .01). These results are consistent with pulmonary microembolization during dialysis with deterioration of gas exchange and Q̇c. These changes appear to occur independent of significant changes in Vt. Possible physiologic mechanisms are discussed.


2011 ◽  
Vol 110 (2) ◽  
pp. 538-544 ◽  
Author(s):  
Elizabeth M. Wagner ◽  
John Jenkins ◽  
Maria Grazia Perino ◽  
Adlah Sukkar ◽  
Wayne Mitzner

Bronchial vascular angiogenesis takes place in a variety of lung inflammatory conditions such as asthma, cystic fibrosis, lung cancer, and chronic pulmonary thromboembolic disease. However, it is unclear whether neovascularization is predominantly appropriate and preserves lung tissue or whether it contributes further to lung pathology through edema formation and inflammation. In the present study we examined airway and lung parenchymal function 14 days after left pulmonary artery ligation. In rats as well as higher mammals, severe pulmonary ischemia results in bronchial vascular proliferation. Using labeled microspheres, we demonstrated an 18-fold increase in systemic blood flow to the ischemic left lung. Additionally, vascular remodeling extended to the tracheal venules, which showed an average 28% increase in venular diameter. Despite this increase in vascularity, airways resistance was not altered nor was methacholine responsiveness. Since these measurements include the entire lung, we suggest that the normal right lung, which represented 78% of the total lung, obscured the ability to detect a change. When functional indexes such as diffusing capacity, in situ lung volume, and vascular permeability of the left lung could be separated from right lung, significant changes were observed. Thus when comparing average left lung values of rats 14 days after left pulmonary artery ligation to left lungs of rats undergoing sham surgery, diffusing capacity of the left lung decreased by 72%, left lung volume decreased by 38%, and the vascular permeability to protein increased by 58%. No significant differences in inflammatory cell recruitment were observed, suggesting that acute ischemic inflammation had resolved. We conclude that despite the preservation of lung tissue, the proliferating bronchial neovasculature may contribute to a sustained decrement in pulmonary function.


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