Measurement of regional bronchial arterial blood flow and bronchovascular resistance in dogs

1982 ◽  
Vol 53 (4) ◽  
pp. 1044-1049 ◽  
Author(s):  
E. M. Baile ◽  
J. M. Nelems ◽  
M. Schulzer ◽  
P. D. Pare

Little is known about normal variations and control of bronchial blood flow and bronchovascular resistance. We have used the reference-flow technique and 15-microns-diameter microspheres to measure bronchial blood flow under physiological conditions. Dogs (n = 13) were anesthetized and ventilated, and their chests were opened. A ligature was placed loosely around the left main pulmonary artery, and the left atrium was cannulated. In six dogs three sets of microspheres were injected simultaneously into the left atrium, and in another seven dogs the three sets of microspheres were injected sequentially at 0.5-h intervals. Prior to each injection measurements of pulmonary arterial, left atrial, and aortic pressures, cardiac output, and blood gases were made. Five seconds after injection the left main pulmonary artery was transiently occluded to prevent recirculation. After the final injection, dogs were killed, the lungs were removed, and the parenchyma was stripped off the large and small airways of the left lung. Knowing the radioactivity in the trachea, bronchi, parenchyma, and in the reference flow blood and also the aortic and left atrial pressures, we calculated bronchial blood flow (ml X min-1 X g dry lung-1) and bronchovascular resistance (cmH2O X ml-1 X min X 100 g dry lung). Results showed that there were no significant differences between the three measurements of bronchial blood flow when microspheres were injected simultaneously or sequentially. Bronchial blood flow to the left lung was 0.4% of cardiac output; 55% of the total flow went to lung parenchyma and 45% to trachea and bronchi. Expressed as flow/g dry lung the greatest flow was to the airways.

2012 ◽  
Vol 66 (3) ◽  
pp. 235
Author(s):  
Yeon-Jee Ko ◽  
Song Soo Kim ◽  
Jin-Hwan Kim ◽  
Jae-Hyeong Park ◽  
Jae-Hwan Lee

1984 ◽  
Vol 56 (5) ◽  
pp. 1289-1293 ◽  
Author(s):  
E. M. Baile ◽  
R. K. Albert ◽  
W. Kirk ◽  
S. Lakshaminarayan ◽  
B. J. Wiggs ◽  
...  

Positive end-expiratory pressure (PEEP) increases pulmonary vascular resistance, but its effect on the bronchial circulation is unknown. We have compared two techniques for measuring bronchial blood flow in anesthetized, open-chest, ventilated dogs at varying levels of PEEP. Bronchial blood flow ( Qbr ) to the left lower lobe (LLL) and trachea was measured with radiolabeled microspheres. Total Qbr was partitioned into tracheal, bronchial, and parenchymal fractions. We also measured the bronchopulmonary anastomotic flow ( Qbra ) by attaching cannulas from the lobar pulmonary artery and vein to reservoirs, interrupting the LLL pulmonary blood flow and collecting the flow going into the reservoirs. We measured Qbr and Qbra in 10 animals ventilated with varying levels of PEEP (3, 10, and 15 cmH2O) applied randomly. Pulmonary venous pressure was kept at 0 cmH2O. There was no difference observed between Qbr and Qbra at PEEP 3 and 10 cmH2O, but at PEEP 15 cmH2O, Qbr was greater than Qbra , suggesting that at low left atrial pressures bronchial blood flow drains mainly to the left atrium, whereas at elevated alveolar pressures a larger fraction empties into the right side of the heart. PEEP decreased LLL Qbr and Qbra (P less than 0.01). That fraction of Qbr going to the trachea did not change with PEEP. However, the bronchial and parenchymal fractions decreased.


1991 ◽  
Vol 70 (5) ◽  
pp. 2120-2125 ◽  
Author(s):  
J. L. Theissen ◽  
H. M. Loick ◽  
B. B. Curry ◽  
L. D. Traber ◽  
D. N. Herndon ◽  
...  

Endotoxin [lipopolysaccharide (LPS)] has been reported to reduce hypoxic pulmonary vasoconstriction and thus increases venous admixture. The time course of this failure of pulmonary blood flow regulation was investigated in six chronically instrumented unanesthetized sheep after infusion of Escherichia coli LPS (1 microgram/kg). The change in left pulmonary arterial blood flow (LPBF, ultrasonic transit time) in response to unilateral lung hypoxia (10 min of N2 alternately to the left and right lungs) was compared before and at various time intervals after the administration of LPS. During baseline conditions, LPBF was 33% of total cardiac output and decreased to 15% when the left lung was ventilated with a hypoxic gas mixture. One hour after endotoxin infusion, LPBF remained at 33% of total cardiac output yet only decreased to 28% during the hypoxic challenge. The response to one-lung hypoxia was still significantly depressed 10 h post-LPS administration. It is concluded that hypoxic pulmonary vasoconstriction is almost completely abolished for a prolonged time period after a small dose of LPS.


2012 ◽  
Vol 2012 ◽  
pp. 1-18 ◽  
Author(s):  
Ming-Jyh Chern ◽  
Ming-Ting Wu ◽  
Sheau-Wei Her

Pulmonary regurgitation (PR) is a common phenomenon in pulmonary arteries in patients after repair of tetralogy of Fallot (TOF). The regurgitation fraction of left pulmonary artery (LPA) is usually greater than right pulmonary artery (RPA) according to clinic data. It may be related to blood flow in pulmonary arteries. Therefore, understanding hemodynamics in pulmonary arteries helps to comprehend the reason. The aim of this study is to use 3D reconstructed pulmonary artery models from magnetic resonance imaging (MRI) and to use numerical approaches for simulation of flow variations in pulmonary arteries after repair of TOF. From the numerical results, the blood flow is influenced by the bifurcation angles and geometry of pulmonary artery. The regurgitation happens first in LPA after repair of TOF due to the small angle between LPA and main pulmonary artery (MPA). The recirculation region which obstructs forward blood flow to the left lung is found in LPA during acceleration of systole. We also analyze the pressure distribution; the extreme pressure variations are in dilation area of MPA. Numerical data including regurgitation in MPA, LPA, and RPA are compared with phase contrast MR measured data. Good agreements are found between numerical results and measured data.


1988 ◽  
Vol 65 (3) ◽  
pp. 1131-1139 ◽  
Author(s):  
C. H. Wu ◽  
D. C. Lindsey ◽  
D. L. Traber ◽  
C. E. Cross ◽  
D. N. Herndon ◽  
...  

Distribution of bronchial blood flow was measured in unanesthetized sheep by the use of two modifications of the microsphere reference sample technique that correct for peripheral shunting of microspheres: 1) A double microsphere method in which simultaneous left and right atrial injections of 15-microns microspheres tagged with different isotopes allowed measurement of both pulmonary blood flow and shunt-corrected bronchial blood flow, and 2) a pulmonary arterial occlusion method in which left atrial injection and transient occlusion of the left pulmonary artery prevented delivery to the lung of microspheres shunted through the peripheral circulation and allowed systemic blood flow to the left lung to be measured. Both methods can be performed in unanesthetized sheep. The pulmonary arterial occlusion method is less costly and requires fewer calculations. The double microsphere method requires less surgical preparation and allows measurement without perturbation of pulmonary hemodynamics. There was no statistically significant difference between bronchial blood flow measured with the two methods. However, total bronchial blood flow measured during pulmonary arterial occlusion (1.52 +/- 0.98% of cardiac output, n = 9) was slightly higher than that measured with the double microsphere method (1.39 +/- 0.88% of cardiac output, n = 9). In another series of experiments in which sequential measurements of bronchial blood flow were made, there was a significant increase of 15% in left lung bronchial blood flow during the first minute of occlusion of the left pulmonary artery. Thus pulmonary arterial occlusion should be performed 5 s after microsphere injection as originally described by Baile et al. (1).(ABSTRACT TRUNCATED AT 250 WORDS)


1988 ◽  
Vol 65 (4) ◽  
pp. 1514-1519 ◽  
Author(s):  
M. Manohar

The present study was carried out 1) to compare blood flow in the costal and crural regions of the equine diaphragm during quiet breathing at rest and during graded exercise and 2) to determine the fraction of cardiac output needed to perfuse the diaphragm during near-maximal exercise. By the use of radionuclide-labeled 15-micron-diam microspheres injected into the left atrium, diaphragmatic and intercostal muscle blood flow was studied in 10 healthy ponies at rest and during three levels of exercise (moderate: 12 mph, heavy: 15 mph, and near-maximal: 19-20 mph) performed on a treadmill. At rest, in eucapnic ponies, costal (13 +/- 3 ml.min-1.100 g-1) and crural (13 +/- 2 ml.min-1.100 g-1) phrenic blood flows were similar, but the costal diaphragm received a much larger percentage of cardiac output (0.51 +/- 0.12% vs. 0.15 +/- 0.03% for crural diaphragm). Intercostal muscle perfusion at rest was significantly less than in either phrenic region. Graded exercise resulted in significant progressive increments in perfusion to these tissues. Although during exercise, crural diaphragmatic blood flow was not different from intercostal muscle blood flow, these values remained significantly less (P less than 0.01) than in the costal diaphragm. At moderate, heavy, and near-maximal exercise, costal diaphragmatic blood flow (123 +/- 12, 190 +/- 12, and 245 +/- 18 ml.min-1.100 g-1) was 143%, 162%, and 162%, respectively, of that for the crural diaphragm (86 +/- 10, 117 +/- 8, and 151 +/- 14 ml.min-1.100 g-1).(ABSTRACT TRUNCATED AT 250 WORDS)


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.


1979 ◽  
Vol 27 (3) ◽  
pp. 260-261 ◽  
Author(s):  
Stanley Giannelli ◽  
E. Foster Conklin ◽  
Robert T. Potter

2007 ◽  
Vol 103 (2) ◽  
pp. 594-599 ◽  
Author(s):  
Jesús Sánchez ◽  
Aigul Moldobaeva ◽  
Jessica McClintock ◽  
John Jenkins ◽  
Elizabeth Wagner

We previously showed increased expression of the ELR+, CXC chemokines in the lung after left pulmonary artery obstruction. These chemokines have been shown in other systems to bind their G protein-coupled receptor, CXCR2, and promote systemic endothelial cell proliferation, migration, and capillary tube formation. In the present study, we blocked CXCR2 in vivo using a neutralizing antibody and also studied mice that were homozygous null for CXCR2. To estimate the extent of neovascularization in this model, we measured systemic blood flow to the left lung 14 days after left pulmonary artery ligation (LPAL). We found blood flow significantly reduced (67% decrease) with neutralizing antibody treatment compared with controls. However, blood flow was not altered in the CXCR2-deficient mice compared with wild-type controls after LPAL. To test for ligand availability, we measured macrophage inflammatory protein (MIP)-2 in lung homogenates after LPAL, because this is the predominant CXC chemokine previously shown to be increased after LPAL ( 22 ). MIP-2 protein was two- to fourfold higher in the left lung relative to the right lung in all treatment groups 4 h after LPAL and this increase did not differ among groups. We speculate that the CXCR2-deficient mice have compensatory mechanisms that mitigate their lack of gene expression and conclude that CXCR2 contributes to chemokine-induced systemic angiogenesis after pulmonary artery obstruction.


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