共查询到20条相似文献,搜索用时 15 毫秒
1.
Laine G. A.; Allen S. J.; Katz J.; Gabel J. C.; Drake R. E. 《Journal of applied physiology》1986,61(5):1634-1638
Pulmonary lymph drains into the thoracic duct and then into the systemic venous circulation. Since systemic venous pressure (SVP) must be overcome before pulmonary lymph can flow, variations in SVP may affect lymph flow rate and therefore the rate of fluid accumulation within the lung. The importance of this issue is evident when one considers the variety of clinical interventions that increase SVP and promote pulmonary edema formation, such as volume infusion, positive-pressure ventilation, and various vasoactive drug therapies. We recorded pulmonary arterial pressure (PAP), left atrial pressure (LAP), and SVP in chronic unanesthetized sheep. Occlusion balloons were placed in the left atrium and superior vena cava to control their respective pressures. The superior vena caval occluder was placed above the azygos vein so that bronchial venous pressure would not be elevated when the balloon was inflated. Three-hour experiments were carried out at various LAP levels with and without SVP being elevated to 20 mmHg. The amount of fluid present in the lung was determined by the wet-to-dry weight ratio method. At control LAP levels, no significant difference in lung fluid accumulation could be shown between animals with control and elevated SVP levels. When LAP was elevated above control a significantly greater amount of pulmonary fluid accumulated in animals with elevated SVP levels compared with those with control SVP levels. We conclude that significant excess pulmonary edema formation will occur when SVP is elevated at pulmonary microvascular pressures not normally associated with rapid fluid accumulation. 相似文献
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Effect of high-frequency oscillation on lung lymph flow 总被引:3,自引:0,他引:3
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Studies in anesthetized animals have shown that the flow rate from lung lymphatics (QL) depends on the pressure at the outflow end of the vessels (Po). We tested this in unanesthetized sheep prepared with chronic lung lymph cannula. We measured QL with the lymph cannula held at various heights above the olecranon and calculated Po as the height + QL X cannula resistance. QL decreased with increases in Po (delta QL/delta Po = -8.2 +/- 6.4 microliter X min-1 X cmH2O-1, mean +/- SD). We increased QL by raising left atrial pressure or infusing Ringer solution or Escherichia coli endotoxin and found that QL was even more sensitive to Po (delta QL/delta Po = -32 +/- 22). Cannula resistance caused a 9-70% reduction in QL. Changes in QL caused by increasing Po were not associated with changes in lymph protein concentration for up to 330 min. This indicates that increases in Po shunt lymph away from cannulated vessels but do not substantially effect microvascular filtration rate. The shunted lymph may flow into other vessels or collect in the lung. We conclude that QL does not accurately represent microvascular filtration rate because it depends on the cannula resistance and position at which the investigator chooses to place the cannula. 相似文献
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Effect of increased bronchial venous pressure on lung lymph flow 总被引:1,自引:0,他引:1
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Kong D Kong X Wang L 《Physiological research / Academia Scientiarum Bohemoslovaca》2006,55(3):253-258
The effect of chronic cardiac lymphatic obstruction on the myocardial synthesis of collagen type I and III was investigated in a rabbit model. In the lymphatic obstruction group (n=16), plasma C-terminal propeptide type I procollagen (PICP) and N-terminal propeptide type III procollagen (PIIINP) were elevated at 7, 14 and 30 days after the operation (p<0.05). The elevated PICP and PIIINP returned to the pre-operation values 60 days after the operation. The myocardial expression of collagen type I and III mRNA were also enhanced in the lymphatic flow obstruction group. Plasma PICP, PIIINP and myocardial collagen type I and III mRNA remained unchanged in the control group (n=16). We concluded that chronic obstruction of cardiac lymph flow leads to enhanced myocardial collagen synthesis in rabbits. The enhanced collagen synthesis starts within seven days after lymphatic obstruction and subsides after 60 days. 相似文献
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Conforti E Fenoglio C Bernocchi G Bruschi O Miserocchi GA 《American journal of physiology. Lung cellular and molecular physiology》2002,282(4):L766-L774
Mild pulmonary interstitial edema was shown to cause fragmentation of interstitial matrix proteoglycans. We therefore studied compartmental fluid accumulation by light and electron microscopy on lungs of anesthetized rabbits fixed in situ by vascular perfusion after 0.5 ml.kg(-1).min(-1) iv saline infusion for 180 min causing approximately 6% increase in lung weight. Morphometry showed that a relevant portion (44%) of extravascular fluid is detected early in the alveolar septa, 85% of this fluid accumulating in the thick portion of the air-blood barrier. The arithmetic mean thickness of the barrier increased in interstitial edema from 1.06 +/- 0.05 (SE) to 1.33 +/- 0.06 microm. The harmonic mean thickness increased from 0.6 +/- 0.03 to 0.86 +/- 0.07 microm, mostly due to thickening of the thin portion causing an increase in gas diffusion resistance. Despite some structural damage, the air-blood barrier displays a relatively high structural resistance providing a safety factor against the development of severe edema. It is suggested that the increase in extra-alveolar perivascular space occurs as a consequence of fluid accumulation in the air-blood barrier. 相似文献
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Effect of edema on the relationship between rate of fluid filtration and vascular pressure was studied in ventilated isolated dog lung lobes blood-perfused at constant flow. Constant rate of lobe weight gain (S), representing transvascular fluid flux, was obtained at different venous pressures (Pv) as Pv was increased stepwise from 2 to 40 and then similarly decreased from 40 to 2 Torr (n = 6). In another group (n = 6), edema was maximized by reversing the sequence of Pv change; S was obtained during similar Pv steps as Pv was decreased from 40 to 2 and then returned to 40 Torr. In both groups, delta S was disproportionately greater for delta Pv at higher Pv's, with S vs. Pv fit by an exponential curve (P less than 0.001). The exponential relationship was independent of lung hydration inasmuch as greater edema on the second limb of Pv change did not alter the curve (P greater than 0.05). At 144% weight gain, interstitial compliance was 55.5 +/- 26.8 ml.100 g-1.Torr-1 (n = 10). Interstitial pressure reportedly remains constant, i.e., fails to increase to further buffer fluid filtration, after transition of the lung interstitium from low to high compliance at approximately 40% lung weight gain. If so, then the exponential S vs. Pv relationship observed in the present study at elevated interstitial compliance does not appear related to tissue pressure-buffering effects. 相似文献
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Neutropenia was produced in goats by injection of either nitrogen mustard, (1.5 mg/kg) or hydroxyurea (200 mg X kg-1 X day-1). A nitrogen mustard (M + E) group (n = 6), a hydroxyurea (H + E) group (n = 5), and a control (E) group (n = 7) were given 1-h infusions of endotoxin (5 micrograms/kg total dose), then monitored for up to 5 h. Postmortem extravascular lung water (EVLW) was significantly higher in the M + E group (14.2 +/- 4.4 ml/kg) and the E group (11.9 +/- 3.9 ml/kg) when compared with a normal control (6.6 +/- 1.3 ml/kg) group that did not receive endotoxin. EVLW in a group made neutropenic with nitrogen mustard (6.7 +/- 1.3 ml/kg) and the H + E (7.9 +/- 1.5 ml/kg) groups were not statistically different from each other or from normal controls. Circulating neutrophil counts averaged 32 +/- 42 cells/microliter in the M + E group and 180 +/- 210 cells/microliter in the H + E group. Only minimal histological changes were seen in the H + E group, but the E and M + E lungs had severe pulmonary edema. We conclude that neutrophils are not required for increased EVLW and decreased arterial O2 partial pressure after endotoxin infusion, and hydroxyurea prevents at least part of the pulmonary edema after endotoxin by a mechanism that is not neutrophil dependent. 相似文献
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Sabbadini M Barisani D Conforti E Marozzi A Ginelli E Miserocchi G Meneveri R 《Biochimica et biophysica acta》2003,1638(2):149-156
To investigate the molecular events taking place during the development of hydraulic interstitial edema, we analyzed by microarray and conventional molecular techniques the variation of gene expression in lung from rabbits treated with slow-rate saline infusions. This analysis indicates that even a condition characterized by a small increase in extravascular water can have a significant influence on the inflammatory milieu. In this regard, cytokines, in particular TNFalpha, can be considered early mediators capable of inducing secondary effects on the injured tissue. Moreover, two MT1 genes were strongly up-regulated, data consistent with their role as protective molecules. 相似文献
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David B Pearse Robert M Searcy Wayne Mitzner Solbert Permutt J T Sylvester 《Journal of applied physiology》2005,99(2):556-563
Ventilation (V) increases lung lymph flow (Ql), but the separate effects of tidal volume (Vt) and frequency (f) and the role of V-induced changes in edema formation are poorly understood. An isolated, in situ sheep lung preparation was used to examine these effects. In eight sheep with f = 10 min(-1), results obtained during 30-min periods with Vt = 5 or 20 ml/kg were compared with values obtained during bracketed 30-min control periods (Vt = 12.5 ml/kg). Eight other sheep with constant Vt (12.5 ml/kg) were studied at f = 5 or 20 min(-1) and compared with f = 10 min(-1). Three additional groups of six sheep were perfused for 100 min with control V (10 ml/kg, 10 min(-1)). Vt was then kept constant or changed to 20 or 3 ml/kg during a second 100-min period. Increases in Vt or f increased Ql and vice versa, without corresponding effects on the rate of edema formation. For the same change in V, changing Vt had a greater effect on Ql than changing f. The change in Ql caused by an increase in Vt was significantly greater after the accumulation of interstitial edema. The change in Ql caused by a sustained increase in Vt was transient and did not correlate with the rate of edema formation, suggesting that V altered Ql through direct mechanical effects on edema-filled compartments and lymphatic vessels rather than through V-induced changes in fluid filtration. 相似文献
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Anglade Daniel; Corboz Michel; Menaouar Ahmed; Parker James C.; Sanou Sagazaga; Bayat Sam; Benchetrit Gila; Grimbert Francis A. 《Journal of applied physiology》1998,84(3):1011-1023
On the basis ofchanges in capillary filtration coefficient(Kfc) in 24 rabbit lungs, we determined whether elevations in pulmonary venouspressure (Ppv) or blood flow (BF) produced differences infiltration surface area in oleic acid-injured (OA) or control (Con)lungs. Lungs were cyclically ventilated and perfused under zone 3 conditions by using blood and 5% albumin with no pharmacological modulation of vascular tone. Pulmonary arterial, venous, and capillary pressures were measured by using arterial, venous, and double occlusion. Before and during eachKfc-measurementmaneuver, microvascular/total vascular compliance was measured by usingvenous occlusion.Kfc was measuredbefore and 30 min after injury, by using a Ppv elevation of 7 cmH2O or a BF elevation from 1 to2 l · min1 · 100 g1 to obtain a similardouble occlusion pressure. Pulmonary arterial pressure increased morewith BF than with Ppv in both Con and OA lungs [29 ± 2 vs. 19 ± 0.7 (means ± SE) cmH2O;P < 0.001]. In OA lungscompared with Con lungs, values ofKfc (200 ± 40 vs. 83 ± 14%, respectively; P < 0.01) and microvascular/total vascular compliance ratio (86 ± 4 vs. 68 ± 5%, respectively; P < 0.01) increased more with BF than with Ppv. In conclusion, for a given OA-induced increase in hydraulic conductivity, BF elevation increased filtration surface area more than did Ppv elevation. The steep pulmonary pressure profile induced by increased BF could result in therecruitment of injured capillaries and could also shift downstream thecompression point of blind (zone 1) and open injured vessels (zone 2). 相似文献
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Jennifer H. Siggers Kritsada Leungchavaphongse Chong Hang Ho Rodolfo Repetto 《Biomechanics and modeling in mechanobiology》2014,13(2):363-378
We present a mathematical model of blood and interstitial flow in the liver. The liver is treated as a lattice of hexagonal ‘classic’ lobules, which are assumed to be long enough that end effects may be neglected and a two-dimensional problem considered. Since sinusoids and lymphatic vessels are numerous and small compared to the lobule, we use a homogenized approach, describing the sinusoidal and interstitial spaces as porous media. We model plasma filtration from sinusoids to the interstitium, lymph uptake by lymphatic ducts, and lymph outflow from the liver surface. Our results show that the effect of the liver surface only penetrates a depth of a few lobules’ thickness into the tissue. Thus, we separately consider a single lobule lying sufficiently far from all external boundaries that we may regard it as being in an infinite lattice, and also a model of the region near the liver surface. The model predicts that slightly more lymph is produced by interstitial fluid flowing through the liver surface than that taken up by the lymphatic vessels in the liver and that the non-peritonealized region of the surface of the liver results in the total lymph production (uptake by lymphatics plus fluid crossing surface) being about 5 % more than if the entire surface were covered by the Glisson–peritoneal membrane. Estimates of lymph outflow through the surface of the liver are in good agreement with experimental data. We also study the effect of non-physiological values of the controlling parameters, particularly focusing on the conditions of portal hypertension and ascites. To our knowledge, this is the first attempt to model lymph production in the liver. The model provides clinically relevant information about lymph outflow pathways and predicts the systemic response to pathological variations. 相似文献
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Parker R. E.; Wickersham N. E.; Roselli R. J.; Harris T. R.; Brigham K. L. 《Journal of applied physiology》1986,60(4):1293-1299
Experiments were conducted on five chronically instrumented unanesthetized sheep to determine the effects of sustained hypoproteinemia on lung fluid balance. Plasma total protein concentration was decreased from a control value of 6.17 +/- 0.019 to 3.97 +/- 0.17 g/dl (mean +/- SE) by acute plasmapheresis and maintained at this level by chronic thoracic lymph duct drainage. We measured pulmonary arterial pressure, left atrial pressure, aortic pressure, central venous pressure, cardiac output, oncotic pressures of both plasma and lung lymph, lung lymph flow rate, and lung lymph-to-plasma ratio of total proteins and six protein fractions for both control base-line conditions and hypoproteinemia base-line conditions. Moreover, we estimated the average osmotic reflection coefficient for total proteins and the solvent drag reflection coefficients for the six protein fractions during hypoproteinemia. Hypoproteinemia caused significant decreases in lung lymph total protein concentration, lung lymph-to-plasma total protein concentration ratio, and oncotic pressures of plasma and lung lymph. There were no significant alterations in the vascular pressures, lung lymph flow rate, cardiac output, or oncotic pressure gradient. The osmotic reflection coefficient for total proteins was found to be 0.900 +/- 0.004 for hypoproteinemia conditions, which is equal to that found in a previous investigation for sheep with a normal plasma protein concentration. Our results suggest that hypoproteinemia does not alter the lung filtration coefficient nor the reflection coefficients for plasma proteins. Possible explanations for the reported increase in the lung filtration coefficient during hypoproteinemia by other investigators are also made. 相似文献
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We have determined the effect of dehydration on regional lung interstitial pressures. We stopped blood flow in the isolated blood-perfused lobe of dog lung at vascular pressure of approximately 4 cmH2O. Then we recorded interstitial pressures by micropuncture at alveolar junctions (Pjct), in perimicrovascular adventitia (Padv), and at the hilum (Phil). After base-line measurements, we ventilated the lobes with dry gas to decrease extravascular lung water content by 14 +/- 5%. In one group (n = 10), at constant inflation pressure of 7 cmH2O, Pjct was 0.2 +/- 0.8 and Padv was -1.5 +/- 0.6 cmH2O. After dehydration the pressures fell to -5.0 +/- 1.0 and -5.3 +/- 1.3 cmH2O, respectively (P less than 0.01), and the junction-to-advential gradient (Pjct-Padv) was abolished. In a second group (n = 6) a combination of dehydration and lung expansion with inflation pressure of 15 cmH2O further decreased Pjct and Padv to -7.3 +/- 0.7 and -7.1 +/- 0.7 cmH2O, respectively. Phil followed changes in Padv. Interstitial compliance was 0.6 at the junctions, 0.8 in adventitia, and 0.9 ml.cmH2O-1.100 g-1 wet lung at the hilum. We conclude, that perialveolar interstitial pressures may provide an important mechanism for prevention of lung dehydration. 相似文献
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Raffaele L Dellacà Emanuela Zannin Giulio Sancini Ilaria Rivolta Biagio E Leone Antonio Pedotti Giuseppe Miserocchi 《Respiratory research》2008,9(1):51