Effect of systemic venous pressure elevation on lymph flow and lung edema formation

Laine, Glen A.; Allen, Steven J.; Katz, Joseph; Gabel, Joseph C.; Drake, R. E.

doi:10.1152/jappl.1986.61.5.1634

Cited by 87 publications

(36 citation statements)

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“…5), at least not with the outflow pressures we applied. These results obtained with non-invasive techniques are similar to those obtained by Drake et al (1985) and Laine, Allen, Katz, Gabel & Drake (1986). They found that flow from cannulated lung lymphatics did not recover during 3 or 6 h periods of elevated outflow pressure in unanaesthetized sheep.…”

Section: Effect Of Outflow Venous Pressuresupporting

confidence: 87%

Lymph Flow Pattern in the Intact Thoracic Duct in Sheep

Onizuka

Flatebø

Nicolaysen

1997

The Journal of Physiology

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To study the lymph flow dynamics in the intact thoracic duct, we applied an ultrasound transit‐time flow probe in seven anaesthetized and four unanaesthetized adult sheep (.60 kg). In unanaesthetized non‐fasting animals we found that lymph flow in the thoracic duct was always regular pulsatile (pulsation frequency, 5.2 ± 0.8 min−1) with no relation to heart or respiratory activity. At baseline the peak level of the thoracic duct pulse flow was 11.6–20.7 ml min−1 with a nadir of 0–3.6 ml min−1. Mean lymph flow was 5.4 ± 3.1 ml min−1. The flow pattern of lymph in the thoracic duct was essentially the same in the anaesthetized animals. In both the anaesthetized and unanaesthetized animals, the lymph flow response to a stepwise increase in the outflow venous pressure showed interindividual variation. Some were sensitive to any increase in outflow venous pressure, but others were resistant in that lymph flow did not decrease until outflow venous pressure was increased to higher levels. This resistance was also observed in the high lymph flow condition produced by fluid infusion in the anaesthetized animal and mechanical constriction of the caudal vena cava in the unanaesthetized animals. Pulsation frequency of the thoracic duct flow initially increased and then decreased with a stepwise increase in the outflow venous pressure. This initial increase might be a compensatory response to maintain lymph flow against elevated outflow venous pressure. To test the effect of long‐term outflow venous pressure elevation in unanaesthetized sheep, outflow venous pressure was increased by inflation of a cuff around the cranial vena cava for 1, 5 or 25 h. The cuff was inflated to a level where lymph flow was reduced. Lymph flow remained low or decreased further during the entire cuff‐inflation period. We calculated the lymph debt caused by the outflow venous pressure elevation and the amount ‘repaid’ when venous pressure returned to normal. Lymph debt for 25 h was 6400 ml but only 200 ml was repaid. Since we observed no visible oedema formation in the lower body of the sheep, the non‐colloidal components of the lymph must have been reabsorbed into the bloodstream, most likely in the lymph nodes.

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Section: Effect Of Outflow Venous Pressuresupporting

confidence: 87%

Lymph Flow Pattern in the Intact Thoracic Duct in Sheep

Onizuka

Flatebø

Nicolaysen

1997

The Journal of Physiology

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“…Thus, the factors that may affect fluid clearance by the lymphatic system (Drake, Adcock, Scott & Gabel, 1982;Drake, Scott & Gabel, 1983;Laine, Allen, Katz, Gabel & Drake, 1986;Frostell, Blomqvist, Hedestierna, Halbig & Pieper, 1987a) appeared to be similar in all four groups.…”

Section: Effects Of Hhs Bolus Injectionmentioning

confidence: 87%

Influence of hypertonic‐hyperoncotic solution and furosemide on canine hydrostatic pulmonary oedema resorption.

Wickerts

Berg

Frostell

et al. 1992

The Journal of Physiology

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SUMMARY1. This study aimed at enhancing the clearance of experimental hydrostatic pulmonary oedema in dogs using hypertonic-hyperoncotic solution (HHS) and furosemide.2. Anaesthetized dogs (n = 20) were mechanically ventilated with a positive endexpiratory pressure of 10 cmH20 (1-0 kPa).3. Hydrostatic pulmonary oedema was induced by inflating a balloon inserted into the left atrium and simultaneously infusing isotonic saline rapidly. Gedema formation was terminated by deflating the balloon and reducing the infusion rate.4. Four groups were studied: A, control; B, furosemide; C, HHS and D, HHS + furosemide. HHS, 6 ml kg-', was given as a bolus injection and furosemide, 1 mg kg-', intravenously as a bolus followed by an infusion of 0 5 mg kg-' h-1. All dogs were studied for 4 h.5. Serum osmolarity, plasma colloid oncotic pressure and diuresis in groups C and D (HHS groups) substantially increased; haemoglobin concentration decreased and pulmonary arterial wedge pressure remained constant.6. Despite the combination of these factors favouring fluid flux from the extravascular to the intravascular compartment, extravascular lung water measured with the double indicator dilution technique decreased no faster in the HHS groups than in the two other groups (from over 26 to approximately 19 ml kg-' in groups A, C and D and to 14-7 in group B (only furosemide)).7. This was confirmed by postmortem gravimetric measurements of extravascular lung water; A, 11-0+5-7; B, 9-7+3-3; C, 10-5+331 and D, 106±+1-8 g kg-'.

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“…The effects of an increase in intrathoracic pressure on lymphatic flow were described a decade ago (51,52). In animal models, raising intrathoracic pressure reduced the lymphatic flow and impaired the clearance of lung edema (53)(54)(55). In our study, we found a positive correlation between the increase of esophageal pressure (i.e., the pleural pressure) and the edema formation rate after aIAP of 20 cm H 2 O (edema formation rate [ml/minute] ϭ 1.7 ϫ ⌬ esophageal pressure ϩ 7.0, r ϭ 0.83, p Ͻ 0.05, data not shown).…”

Section: Oleic Acid-injured Lungmentioning

confidence: 99%

An Increase of Abdominal Pressure Increases Pulmonary Edema in Oleic Acid–induced Lung Injury

Quintel

Pelosi

Caironi

et al. 2004

Am J Respir Crit Care Med

169

108

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Increased abdominal pressure is common in intensive care unit patients. To investigate its impact on respiration and hemodynamics we applied intraabdominal pressure (aIAP) of 0 and 20 cm H 2 O (pneumoperitoneum) in seven pigs. The whole-lung computed tomography scan and a complete set of respiratory and hemodynamics variables were recorded both in healthy lung and after oleic acid (OA) injury. In healthy lung, aIAP 20 cm H 2 O significantly lowered the gas content, leaving the tissue content unchanged. In OAinjured lung at aIAP 0 cm H 2 O, the gas content significantly decreased compared with healthy lung. The excess tissue mass (edema) amounted to 30 Ϯ 24% of the original tissue weight (455 Ϯ 80 g). The edema was primarily distributed in the base regions and was not gravity dependent. Heart volume, central venous, pulmonary artery, wedge, and systemic arterial pressures significantly increased. At aIAP 20 cm H 2 O in OA-injured lung, the central venous and pulmonary artery pressures further increased. The gas content further decreased, and the excess tissue mass rose up to 103 Ϯ 37% (tissue weight 905 Ϯ 134 g), with homogeneous distribution along the cephalocaudal and sternovertebral axis. We conclude that in OAinjured lung, the increase of IAP increases the amount of edema.Keywords: intraabdominal pressure; acute respiratory distress syndrome; pulmonary edema; lung mechanics; computed tomography scanThe importance of intraabdominal pressure (IAP) in acute lung injury and acute respiratory distress syndrome has been recently suggested (1). For a long time any change in respiratory mechanics in patients with acute lung injury/acute respiratory distress syndrome was attributed to lung mechanics, whereas chest wall mechanics was assumed to be normal. However, few studies in which chest wall elastance was actually measured have showed that it was abnormal in a substantial proportion of patients with acute lung injury/acute respiratory distress syndrome (2-4). We (5) and others (6) have described different chest wall mechanics in patients with pulmonary and extrapulmonary acute respiratory distress syndrome, mainly due to different IAP values.However, apart from respiratory mechanics, the increased intrathoracic pressure caused by chest wall impairment may have important consequences on hemodynamics (7). We investigated the effect of changing IAP during controlled mechanical ventilation in healthy and diseased lungs. Surprisingly, the increase of IAP had an unexpected impact on lung edema, likely related to its formation and clearance. We wish to report our findings and METHODS(Additional details about Methods are provided in an online supplement.)The study group consisted of seven anesthetized and paralyzed domestic pigs (41 Ϯ 4 kg) ventilated throughout the experiment in supine position, with a Vt of 12 ml/kg, respiratory rate of 12-14 breaths/minute, positive end-expiratory pressure of 5 cm H 2 O, and Fi O 2 of 1.0. The animals were fully instrumented for hemodynamic monitoring (carotid artery, right atrium, mea...

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Effect of systemic venous pressure elevation on lymph flow and lung edema formation

Cited by 87 publications

References 0 publications

Lymph Flow Pattern in the Intact Thoracic Duct in Sheep

Lymph Flow Pattern in the Intact Thoracic Duct in Sheep

Influence of hypertonic‐hyperoncotic solution and furosemide on canine hydrostatic pulmonary oedema resorption.

An Increase of Abdominal Pressure Increases Pulmonary Edema in Oleic Acid–induced Lung Injury

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