Changes in the spatial distribution of pulmonary blood flow during the fetal/neonatal transition: an in vivo study in the rabbit

1989 ◽  
Vol 6 (4) ◽  
pp. 213-222 ◽  
Author(s):  
Jill Lipsett ◽  
Kerri Hunt ◽  
Colin Carati ◽  
Bren Gannon
1988 ◽  
Vol 151 (1) ◽  
pp. 139-141 ◽  
Author(s):  
AS Brody ◽  
SH Embury ◽  
WC Mentzer ◽  
ML Winkler ◽  
CA Gooding

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.


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.


2002 ◽  
Vol 26 (5) ◽  
pp. 296-298 ◽  
Author(s):  
Kei Koga ◽  
Masatoshi Naito ◽  
Yuichiro Akiyoshi ◽  
Isao Asayama ◽  
Kei Shiramizu ◽  
...  

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.


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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