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.

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.

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.

Partial anomalous left pulmonary artery: report of two cases and review of literature

2014 ◽  
Vol 25 (5) ◽  
pp. 1012-1014 ◽  
Author(s):  
Supratim Sen ◽  
David S. Winlaw ◽  
Gary F. Sholler
Keyword(s):  
Pulmonary Artery ◽  
Lower Lobe ◽  
Left Pulmonary Artery ◽  
Primary Diagnosis ◽  
Left Lower Lobe ◽  
Lobe Bronchus ◽  
First Child ◽  
Right Pulmonary Artery ◽  
The Right ◽  
Aortic Arch Hypoplasia

AbstractWe describe two cases of anomalous origin of the left lower-lobe pulmonary artery from the right pulmonary artery. The primary diagnosis was mitral atresia, hypoplastic left ventricle, aortic arch hypoplasia in the first child, and tetralogy of Fallot in the second. In both cases, the pulmonary trunk gave rise to a left pulmonary artery in the normal position. In addition, a second branch of the left pulmonary artery arose from the right pulmonary artery, and passed posterior and inferior to the left main or upper-lobe bronchus to supply the left lower lobe. In this review, we compare our findings with previously reported examples of this extremely rare cardiac malformation, and discuss possible embryological explanations for the lesion.

Abstract 12430: Vicious Circle Between Progressive Right Ventricular Dilatation and Pulmonary Regurgitation in Patients After Tetralogy of Fallot Repair? Right Heart Enlargement Promotes Flow Reversal in the Left Pulmonary Artery

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Atsuko Kato ◽  
Christian Drolet ◽  
Shi-Joon Yoo ◽  
Andrew Redington ◽  
Lars Grosse-Wortmann
Keyword(s):  
Pulmonary Artery ◽  
Tetralogy Of Fallot ◽  
Left Lung ◽  
Pulmonary Regurgitation ◽  
Left Pulmonary Artery ◽  
Flow Reversal ◽  
Left Hemithorax ◽  
Forward Flow ◽  
Lung Area ◽  
The Right

Introduction: The left pulmonary artery (LPA) contributes more than the right (RPA) to total pulmonary regurgitation (PR) in patients after tetralogy of Fallot (TOF) repair, but the mechanism of this difference is not well known. We hypothesized that unilaterally increased pulmonary vascular resistance (PVR), resulting from lung compression by the enlarged and levorotated heart leads to greater PR in the LPA. This study aimed to analyze the interplay between heart and lung size, mediastinal geometry, and differential PR. Methods: This is a single-center retrospective analysis of 50 magnetic resonance studies in patients after TOF repair. Patients with more than mild discrete branch pulmonary artery stenosis were excluded. Blood flow was measured by phase-contrast velocity encoding within the branch pulmonary arteries. On the axial image with the largest total cardiac surface area, cardiac angle (α) between the thoracic anterior-posterior line and the interventricular septum, right and left lung areas as well as right and left hemithorax areas were measured (Figure). Results: There was no difference in LPA and RPA diameters. The LPA showed significantly less total forward flow (p=0.04), smaller net forward flow (p=<0.001), and greater RF (p=0.001) than the RPA. Left lung area was smaller than the right (p<0.001). RVEDVi correlated with LPA RF (R=0.48, p<0.001), but not with RPA RF. Larger RVEDVi correlated with a larger α angle (R=0.46, p<0.001), i.e. a more leftward cardiac axis and with smaller left lung area (R=-0.58, p<0.001). LPA RF, but not RPA RF, correlated inversely with left lung area indexed to the left hemithorax area (R=-0.34, p=0.02). Conclusions: An enlarged and levorotated heart - as a result of PR - is associated with smaller left lung size, and augments diastolic flow reversal in the LPA, presumably via increased left PVR. By imposing a further volume load on the RV, LPA regurgitation may thus close a positive feed-back loop of PR and RV dilatation.

Breathing frequency responses to pulmonary CO2 in an isolated lobe of the canine lung

1979 ◽  
Vol 47 (6) ◽  
pp. 1201-1206 ◽  
Author(s):  
J. O. Nilsestuen ◽  
R. L. Coon ◽  
F. O. Igler ◽  
E. J. Zuperku ◽  
J. P. Kampine
Keyword(s):  
Airway Pressure ◽  
Left Lung ◽  
Lower Lobe ◽  
Stretch Receptor ◽  
Left Lower Lobe ◽  
Breathing Frequency ◽  
Frequency Responses ◽  
Mechanical Effects ◽  
Frequency Changes ◽  
The Right

Recent studies have indicated that the breathing frequency responses to inspired CO2 in part result from changes in pulmonary stretch receptor activity. Pulmonary CO2 may alter frequency by direct inhibition of stretch receptor discharge, or secondarily, by changes in airway mechanics. The vascularly isolated left lower lobe (LLL) of the canine lung was used to determine the effect of hypocapnic airway constriction on the pulmonary CO2 reflex. The upper and middle lobes of the left lung were removed and the right vagus nerve sectioned. Blood was recirculated through the LLL. Diaphragm electromyogram was used as an index of respiratory center activity and to trigger ventilation of the left lower lobe. Lobar hypocapnia increased peak airway pressure and reduced respiratory rate. However, infusion of isoproterenol or the use of a mechanical overflow system to block the airway pressure response prevented the frequency changes associated with CO2. Although both the direct and mechanical effects of CO2 on stretch receptors may contribute to the reflex, in the LLL preparation the mechanical effects predominate.

Bronchial Obstruction Due to Pulmonary Artery Anomalies. I. Vascular Sling

PEDIATRICS ◽  
1958 ◽  
Vol 22 (1) ◽  
pp. 48-48
Keyword(s):  
Pulmonary Artery ◽  
Clinical Symptoms ◽  
Early Recognition ◽  
Vascular Ring ◽  
Left Lung ◽  
Posterior Wall ◽  
Left Pulmonary Artery ◽  
Bronchial Obstruction ◽  
Vascular Sling ◽  
The Right

The authors report three cases of respiratory embarrassment in infants from compression of the right bronchus and trachea by a "vascular sling" formed by an aberrant left pulmonary artery coursing anterior to the right main-stem bronchus and posterior to the trachea. Five similar cases have been described in earlier literature. The embryologic origin of this anomaly appears to be a disturbed time-sequence in the growth and union of the left pulmonary artery and the left lung bud. The clinical symptoms are those of respiratory distress in the neonatal period produced by tracheobronchial compression, associated with obstructive emphysema of the right lung. Bronchoscopic examination reveals extrinsic pressure on the right bronchus and posterior wall of the trachea. The esophagram does not reveal any posterior indentation and is thereby helpful in distinguishing this entity from the more common "vascular ring" which is a systemic arterial malformation causing constriction of the trachea and esophagus. Early recognition of an anomalous left pulmonary artery is particularly important in view of the fact that the condition can be corrected surgically.

Quantification of pulmonary vascular occlusion in dogs by use of the diffusing capacity

1988 ◽  
Vol 64 (3) ◽  
pp. 1229-1238 ◽  
Author(s):  
T. R. Chappell ◽  
S. S. Cassidy ◽  
F. Schwiep ◽  
M. Ramanathan ◽  
R. L. Johnson
Keyword(s):  
Pulmonary Artery ◽  
Arterial Occlusion ◽  
Vascular Occlusion ◽  
Left Pulmonary Artery ◽  
Diffusing Capacity ◽  
Right Pulmonary Artery ◽  
Fractional Reduction ◽  
Pulmonary Arterial ◽  
High Concentrations ◽  
The Right

The purpose of these experiments was to quantify stagnant intrapulmonary blood caused by a pulmonary arterial occlusion (PAO). The hypothesis was that the diffusing capacity of the lung for CO (DLCO) would be altered little by PAO when measured with the usual inspired concentrations (0.3%) of CO, since stagnant blood distal to the occlusion takes up CO for 20 s or more before significant CO backpressure would develop. However, higher levels of CO (i.e., greater than or equal to 3%) would equilibrate faster with capillary blood (within 5-10 s), and DLCO measured 10-20 s subsequent to the high CO exposure would reflect only the DLCO in the unoccluded regions. Thus the fractional reduction in DLCO measured with 3% CO, with respect to that measured with 0.3% CO, should be related to the fractional occlusion of the pulmonary artery in a predictable way. We occluded the right pulmonary artery (RPAO), the left pulmonary artery (LPAO), or the left lower lobar artery (LLPAO) and found that DLCO measured during rebreathing a 0.3% CO mixture was 80, 87, and 94%, respectively, of the preocclusion value, whereas the DLCO measured during rebreathing a 3.3% CO mixture was 59, 73, and 87% of the preocclusion value. A computer model was developed to predict the reduction in DLCO at different levels of CO exposure that would be caused by varying fractions of PAO. Our data indicated that RPAO corresponded to a 42% vascular occlusion, LPAO a 35% occlusion, and LLPAO a 20% occlusion. Measurement of DLCO using low and high concentrations of CO might be useful in assessing the fraction of vascular bed occluded and in following noninvasively the course of vascular occlusion in a variety of pulmonary diseases.

scholarly journals Left pulmonary artery agenesis with pulmonary hypoplasia in an elderly patient: a rare case report

2013 ◽  
Vol 12 (4) ◽  
pp. 462-466
Author(s):  
A Santra ◽  
R Padhi ◽  
P Dutta ◽  
R Manjhi ◽  
S Pothal ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Aortic Arch ◽  
Rare Case ◽  
Medical Science ◽  
Left Lung ◽  
Left Pulmonary Artery ◽  
Lung Hypoplasia ◽  
Rare Case Report ◽  
The Right ◽  
Pulmonary Artery Agenesis

Proximal interruption of the unilateral pulmonary artery is a rare congenital anomaly, which is often associated with other cardiovascular abnormalities. It is usually diagnosed in children but rarely discovered in adulthood as an isolated phenomenon, occurring more frequently on the right side and is often associated with a contralateral aortic arch. We are presenting a rare case of a sixty year old male who was diagnosed with left lung hypoplasia due to proximal interruption of left pulmonary artery with left sided aortic arch without any associated cardiovascular anomalies. DOI: http://dx.doi.org/10.3329/bjms.v12i4.13689 Bangladesh Journal of Medical Science Vol. 12 No. 04 October ’13 Page 462-466

Incidental finding of pulmonary arterial sling during patent ductus arteriosus surgery in a patient with Mowat–Wilson syndrome

2018 ◽  
Vol 28 (8) ◽  
pp. 1074-1076 ◽  
Author(s):  
Juan D. Cano Sierra ◽  
Camilo F. Mestra ◽  
Miguel A. Ronderos Dumit
Keyword(s):  
Pulmonary Artery ◽  
Incidental Finding ◽  
Ductus Arteriosus ◽  
Left Lung ◽  
Posterior Wall ◽  
Left Pulmonary Artery ◽  
Genetic Condition ◽  
Right Pulmonary Artery ◽  
Pulmonary Arterial ◽  
The Right

AbstractMowat–Wilson syndrome is a genetic condition due to a mutation in the ZEB2 gene; it affects many systems including the cardiovascular system. The pulmonary arterial sling originates from a failure of development of the proximal portion of the left sixth aortic arch, resulting in an anomalous left pulmonary artery origin from the posterior wall of the right pulmonary artery and the left pulmonary artery crossing to the left lung between the trachea and the oesophagus. We present a 4-month-old infant with Mowat–Wilson syndrome and left pulmonary arterial sling, and discuss the association of these two rare conditions. Pulmonary arterial sling is significantly more frequent in patients with Mowat–Wilson syndrome than in the general population.

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.

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