scholarly journals Vertical gradients in regional lung density and perfusion in the supine human lung: the Slinky effect

2007 ◽  
Vol 103 (1) ◽  
pp. 240-248 ◽  
Author(s):  
Susan R. Hopkins ◽  
A. Cortney Henderson ◽  
David L. Levin ◽  
Kei Yamada ◽  
Tatsuya Arai ◽  
...  

In vivo radioactive tracer and microsphere studies have differing conclusions as to the magnitude of the gravitational effect on the distribution of pulmonary blood flow. We hypothesized that some of the apparent vertical perfusion gradient in vivo is due to compression of dependent lung increasing local lung density and therefore perfusion/volume. To test this, six normal subjects underwent functional magnetic resonance imaging with arterial spin labeling during breath holding at functional residual capacity, and perfusion quantified in nonoverlapping 15 mm sagittal slices covering most of the right lung. Lung proton density was measured in the same slices using a short echo 2D-Fast Low-Angle SHot (FLASH) sequence. Mean perfusion was 1.7 ± 0.6 ml·min−1·cm−3 and was related to vertical height above the dependent lung (slope = −3%/cm, P < 0.0001). Lung density averaged 0.34 ± 0.08 g/cm3 and was also related to vertical height (slope = −4.9%/cm, P < 0.0001). By contrast, when perfusion was normalized for regional lung density, the slope of the height-perfusion relationship was not significantly different from zero ( P = 0.2). This suggests that in vivo variations in regional lung density affect the interpretation of vertical gradients in pulmonary blood flow and is consistent with a simple conceptual model: the lung behaves like a Slinky (Slinky is a registered trademark of Poof-Slinky Incorporated), a deformable spring distorting under its own weight. The greater density of lung tissue in the dependent regions of the lung is analogous to a greater number of coils in the dependent portion of the vertically oriented spring. This implies that measurements of perfusion in vivo will be influenced by density distributions and will differ from excised lungs where density gradients are reduced by processing.

1986 ◽  
Vol 71 (s15) ◽  
pp. 36P-36P ◽  
Author(s):  
A.H. Kendrick ◽  
A. Rozkovec ◽  
M. Papouchado ◽  
J. West ◽  
J.E. Bees ◽  
...  

Author(s):  
Björn Wieslander ◽  
Joao Génio Ramos ◽  
Malin Ax ◽  
Johan Petersson ◽  
Martin Ugander

Abstract Background Body position can be optimized for pulmonary ventilation/perfusion matching during surgery and intensive care. However, positional effects upon distribution of pulmonary blood flow and vascular distensibility measured as the pulmonary blood volume variation have not been quantitatively characterized. In order to explore the potential clinical utility of body position as a modulator of pulmonary hemodynamics, we aimed to characterize gravitational effects upon distribution of pulmonary blood flow, pulmonary vascular distension, and pulmonary vascular distensibility. Methods Healthy subjects (n = 10) underwent phase contrast cardiovascular magnetic resonance (CMR) pulmonary artery and vein flow measurements in the supine, prone, and right/left lateral decubitus positions. For each lung, blood volume variation was calculated by subtracting venous from arterial flow per time frame. Results Body position did not change cardiac output (p = 0.84). There was no difference in blood flow between the superior and inferior pulmonary veins in the supine (p = 0.92) or prone body positions (p = 0.43). Compared to supine, pulmonary blood flow increased to the dependent lung in the lateral positions (16–33%, p = 0.002 for both). Venous but not arterial cross-sectional vessel area increased in both lungs when dependent compared to when non-dependent in the lateral positions (22–27%, p ≤ 0.01 for both). In contrast, compared to supine, distensibility increased in the non-dependent lung in the lateral positions (68–113%, p = 0.002 for both). Conclusions CMR demonstrates that in the lateral position, there is a shift in blood flow distribution, and venous but not arterial blood volume, from the non-dependent to the dependent lung. The non-dependent lung has a sizable pulmonary vascular distensibility reserve, possibly related to left atrial pressure. These results support the physiological basis for positioning patients with unilateral pulmonary pathology with the “good lung down” in the context of intensive care. Future studies are warranted to evaluate the diagnostic potential of these physiological insights into pulmonary hemodynamics, particularly in the context of non-invasively characterizing pulmonary hypertension.


1980 ◽  
Vol 49 (5) ◽  
pp. 834-840 ◽  
Author(s):  
A. B. Malik ◽  
H. van der Zee ◽  
P. H. Neumann ◽  
N. B. Gertzberg

Regional pulmonary blood flow was determined in dogs during varying degrees of pulmonary edema induced by infusing 179.2-659.4 ml/kg normal saline over 2-3 h. Pulmonary hemodynamics and regional blood flows were measured during the base-line period and at 30 min postinfusion. The degree of pulmonary edema was determined by the final extravascular lung water-to-bloodless dry lung weight ratio (W/D). In dogs developing gross alveolar edema (W/D of 10.70 +/- 0.88 vs. 3.10 +/- 0.30 in controls), the blood flow was shifted to either upper or dependent lung regions. The shift to the upper regions was associated with an increased (P < 0.05) pulmonary arterial pressure (Ppa), whereas the shift to the dependent lung was not associated with a significant change in Ppa. Breathing 100% O2 did not prevent these shifts, suggesting that they were not due to localized hypoxic pulmonary vasoconstriction. The flow distribution patterns were also not related to regional differences in edema. In contrast to the changes during fulminant edema, blood flow distribution did not change after moderate levels of pulmonary edema (W/D of 6.03 0.69), suggesting that gross alveolar flooding is required for a redistribution of pulmonary blood flow. Flow redistribution to the upper lung during airway flooding may be due to increase in Ppa, whereas the increased flow in the dependent lung during the same degree of edema may be due to "bulging" of alveolar vessels into the air spaces, secondary to a decrease in surface activity.


2015 ◽  
Vol 308 (12) ◽  
pp. L1224-L1236 ◽  
Author(s):  
Yoshiko Kawai ◽  
Kumiko Ajima ◽  
Maki Kaidoh ◽  
Masao Sakaguchi ◽  
Satoshi Tanaka ◽  
...  

To further examine the validity of the proposed concept of pulmonary blood flow-dependent CO2 gas excretion in the lungs, we investigated the effects of intramediastinal balloon catheterization-, pulmonary artery catheterization-, or isoprenaline (ISP)-induced changes in pulmonary blood flow on the end-expiratory CO2 gas pressure (PeCO2), the maximal velocity of the pulmonary artery (Max Vp), systemic arterial pressure, and heart rate of anesthetized rabbits. We also evaluated the changes in the PeCO2 in clinical models of anemia or pulmonary embolism. An almost linear relationship was detected between the PeCO2 and Max Vp. In an experiment in which small pulmonary arteries were subjected to stenosis, the PeCO2 fell rapidly, and the speed of the reduction was dependent on the degree of stenosis. ISP produced significant increases in the PeCO2 of the anesthetized rabbits. Conversely, treatment with piceatannol or acetazolamide induced significant reductions in the PeCO2. Treatment with a cell surface F1/FO ATP synthase antibody caused significant reductions in the PeCO2 itself and the ISP-induced increase in the PeCO2. Neither the PeCO2 nor SAP was significantly influenced by marked anemia [%hematocrit (Ht), 70∼47%]. On the other hand, in the presence of less severe anemia (%Ht: 100∼70%) both the PeCO2 and SAP fell significantly when the rabbits' blood viscosity was decreased. The rabbits in which pulmonary embolisms were induced demonstrated significantly reduced PeCO2 values, which was compatible with the lowering of their Max Vp. In conclusion, we reaffirm the validity of the proposed concept of CO2 gas exchange in the lungs.


2010 ◽  
Vol 108 (2) ◽  
pp. 422-429 ◽  
Author(s):  
Torsten Richter ◽  
Ralf Bergmann ◽  
Jens Pietzsch ◽  
Inge Közle ◽  
Frank Hofheinz ◽  
...  

Using small animal PET with 68Ga-radiolabeled human albumin microspheres (Ga-68-microspheres), we investigated the effect of posture on regional pulmonary blood flow (PBF) in normal rats. This in vivo method is noninvasive and quantitative, and it allows for repeated longitudinal measurements. The purpose of the experiment was to quantify spatial differences in PBF in small animals in different postures. Two studies were performed in anesthetized, spontaneously breathing Wistar rats. Study 1 was designed to determine PBF in the prone and supine positions. Ga-68-microspheres were given to five prone and eight supine animals. We found that PBF increased in dorsal regions of supine animals (0.75) more than in prone animals (0.70; P = 0.037), according to a steeper vertical gradient of flow in supine than in prone animals. No differences in spatial heterogeneity were detected. Study 2 was designed to determine the effects of tissue distribution on PBF measurements. Because microspheres remained fixed in the lung, PET was performed on animals in the position in which they received Ga-68-microsphere injections and thereafter in the opposite posture. The distribution of PBF showed a preference for dorsal regions in both positions, but the distribution was dependent on the position during administration of the microspheres. We conclude that PET using Ga-68-microspheres can detect and quantify regional PBF in animals as small as the rat. PBF distributions differed between the prone and supine postures and were influenced by the distribution of lung tissue within the thorax.


1989 ◽  
Vol 76 (6) ◽  
pp. 673-676 ◽  
Author(s):  
A. H. Kendrick ◽  
A. Rozkovec ◽  
M. Papouchado ◽  
J. West ◽  
G. Laszlo

1. Resting pulmonary blood flow (Q.), using the uptake of the soluble inert gas Freon-22 and an indirect estimate of lung tissue volume, has been estimated during breath-holding (Q.c) and compared with direct Fick cardiac output (Q.f) in 16 patients with various cardiac disorders. 2. The effect of breath-hold time was investigated by comparing Q.c estimated using 6 and 10 s of breath-holding in 17 patients. Repeatability was assessed by duplicate measurements of Q.c in the patients and in six normal subjects. 3. Q.c tended to overestimate Q.f, the bias and error being 0.09 l/min and 0.59, respectively. The coefficient of repeatability for Q.c in the patients was 0.75 l/min and in the normal subjects was 0.66 1/min. For Q.f it was 0.72 l/min. There was no significant difference in Q.c measured at the two breath-hold times. 4. The technique is simple to perform, and provides a rapid estimate of Q., monitoring acute and chronic changes in cardiac output in normal subjects and patients with cardiac disease.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Daniel Biermann ◽  
Alexandra Eder ◽  
Hatim Seoudy ◽  
Florian Arndt ◽  
Tillmann Schuler ◽  
...  

Introduction: Fontan palliation is the treatment of choice for patients with morphological or functional univentricular hearts. The unphysiologic and non-pulsatile pulmonary blood flow results in multiorgan complications and a poor long-term outcome. We evaluated graft survival and histomorphology of a pulsatile Fontan conduit generated from Engineered Heart Tissue (EHT) after implantation in a rat model. Hypothesis: We hypothesized that EHT matures and remains contractile in the setting of venous (Fontan-like) preload. Methods: EHT was generated from ventricular cardiomyocytes of neonatal Wistar rats, fibrinogen, thrombin and DMEM. After culture for 14 days constructs were implanted around the right superior vena cava of Wistar rats (n=12, 300-350 g). Immunosupression was achieved by daily subcutaneous injection of Cyclosporin A (25 mg/kg BW) and Methylprednisolone (2 mg/kg BW). MRI (Bruker) was used to assess condensation of EHTs in vivo. Animals were euthanized after 7, 14, 28 and 56 days postoperatively for histomorphological analysis. Transmission electron microscopy was used to evaluate sarcomeric integrity of cardiomyocytes within the construct. Results: In culture, EHTs started beating around day 8 and remained contractile in vivo throughout the experiment (d7=3/3, d14=2/3, d28=3/3, d56=2/3). All animals survived circumferential implantation of EHTs around the right SVC via a right thoracotomy. MRI (d14, n=3) revealed no constriction or stenosis of the SVC by the constructs. Hematoxylin and Eosin staining showed densely packed bundles of cardiomyocytes within the EHT conduit and intense vascularisation. Immunolabeling of actinin and connexin 43 indicated adequate maturation of cardiomyocytes after grafting around the right SVC in rats. Conclusions: EHTs placed around the superior caval vein of Wistar rats survive and contract for a considerable time after implantation. Histomorphology revealed a matured phenotype of grafted cardiomyocytes and an adequate vascularisation. The functional benefit of a contractile neo-ventricle to propel pulmonary blood flow in Fontan patients remains to be evaluated.


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