Regional edema formation in isolated perfused dog lungs.

Hales, Charles A.; Kanarek, David J.; Ahluwalia, B.; Latty, A; Erdmann, John F.; Javaheri, Shahrokh; Kazemi, Homayoun

doi:10.1161/01.res.48.1.121

Cited by 29 publications

(7 citation statements)

References 10 publications

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“…Consequently, it did not accumulate preferentially in the dependent lung regions. This finding is in accordance with previous reports obtained in a number of animal experiments of respiratory failure using different measurement techniques [19][20][21] and in cardiogenic pulmonary oedema [22], where a nongravitational distribution of oedema has been described. The reasons why oedema does not distribute according to the gravity are substantially unknown; however, it appears that the primary mechanism leading to oedema, at least in ARDS, acts equally in each part of the lung and that oedema cannot move freely through the interstitial space.…”

Section: Lung-structure Function Relationships In Early Ards: Homogensupporting

confidence: 93%

Computed tomography in adult respiratory distress syndrome: what has it taught us?

Pelosi¹,

Crotti²,

Brazzi³

et al. 1996

Eur Respir J

117

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Computed tomography (CT) has played an important role in improving our knowledge of the pathophysiology of the adult respiratory distress syndrome (ARDS), and in determining the morphological and functional relationships of different manoeuvres commonly used in the therapeutic management of this syndrome (changes in body position, application of positive end-expiratory pressure (PEEP) and mechanical ventilation).During the early phase of the disease, the ARDS lung is characterized by a homogenous alteration of the vascular permeability. Thus, oedema accumulates evenly in all lung regions with a nongravitational distribution (homogenous lung). The increased lung weight, due to increased oedema, causes a collapse of the lung regions along the vertical axis, through the transmission of hydrostatic forces (compression atelectasis). Thus, the lesions appear mainly in the dependent lung regions (dishomogeneous lung). During inspiration, at plateau pressure, the pulmonary units reopen and, if the PEEP applied is adequate, they stay open during the following expiration. Adequate PEEP is equal to or higher than the hydrostatic forces compressing that unit. Prone position is another manoeuvre which allows previously collapsed lung regions to reopen and, conversely, compresses previously aerated regions, reversing the distribution of gravitational forces. During late ARDS, there is less compression atelectasis and the lung undergoes structural changes, due to the reduced amount of oedema. This is usually associated with CO 2 retention and the development of emphysema-like lesions.In conclusion, computed tomography is not only a research tool, but a useful technique which allows a better understanding of the progressive change in strategy needed to ventilate the adult respiratory distress syndrome lung at different stages of the disease. Eur Respir J., 1996Respir J., , 9, 1055 In the last 10 yrs, the use of computed tomography (CT) in the clinical evaluation of thoracic diseases has rapidly gained popularity and CT has become firmly established as an important research and diagnostic modality [1]. In fact, CT makes it possible to obtain cross-sectional imaging of the lung, so that virtually all intrathoracic pathological conditions can be evaluated. In particular, CT has played an important role in improving our knowledge of the pathophysiology of the adult respiratory distress syndrome (ARDS) and in determining the morphological and functional relationships of different manoeuvres commonly used in the therapeutic management of this syndrome [2].ARDS refers to a generalized inflammation of the lung parenchyma, caused by different diseases. ARDS is characterized by diffuse pulmonary infiltrates, decreased respiratory compliance and severe hypoxaemia, barely responsive to the administration of high inspiratory oxygen concentrations [3]. Moreover, the pathological characteristics of ARDS may change during the course of the disease, from oedema to fibrosis and disruption of alveolar septa [4].The purpose of this revi...

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Section: Lung-structure Function Relationships In Early Ards: Homogensupporting

confidence: 93%

Computed tomography in adult respiratory distress syndrome: what has it taught us?

Pelosi¹,

Crotti²,

Brazzi³

et al. 1996

Eur Respir J

117

View full text Add to dashboard Cite

show abstract

“…The fractional blood flow related to the fractional weight of the longitudinal slices increases from apex to bases, reflecting either the capillary density or diameter per unit of tissue. The nongravitational distribution of edema, as observed in this study, has been found both in patients (21) and in animal models (22,23). Therefore, it is possible that at first the edema increases according to the flow distribution.…”

Section: Oleic Acid-injured Lungsupporting

confidence: 73%

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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“…The loss of vasoconstrictor ability was not unique to hypoxia, however, as the postendotoxin lung vessels also failed to constrict to A II and PGF2, infusions (Table I). Mean wet-to-bloodless dry weight ratios in three of these lungs was 3.11, which is normal in our laboratory (28), suggesting the pulmonary vascular hyporesponsivity In association with this hyporesponsivity there was a rise in prostacyclin from nondetectable levels in seven of eight dogs before endotoxin and at 5 min after endotoxin to a mean of 360 pg/ml (± 130 SEM) (P < 0.01) with prostacyclin now detectable in all eight dogs (Fig. 2).…”

Section: Resultssupporting

confidence: 56%

Role of Thromboxane and Prostacyclin in Pulmonary Vasomotor Changes after Endotoxin in Dogs

Hales¹,

Sonne²,

Peterson³

et al. 1981

J. Clin. Invest.

139

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A B S T R A C T Cyclooxygenase inhibitors prevent the pulmonary vasomotor changes in response to low-dose endotoxin. We, therefore, explored the role of two highly vasoactive prostanoids, thromboxane A2, a vasoconstrictor, and prostacyclin, a vasodilator, in the transient pulmonary vasoconstriction and subsequent loss of alveolar hypoxis vasoconstriction (AHPV) that follows endotoxin. AHPV was tested in the dog with a double-lumened endotracheal tube allowing ventilation of one lung with nitrogen as a hypoxic challenge while the other lung was ventilated with oxygen to maintain systemic oxygenation. Relative distribution of perfusion to the two lungs was assessed with intravenous 133Xe and external scintillation detectors. The stable metabolites of thromboxane and prostacyclin, i.e., thromboxane B2 and 6-keto-prostaglandin F1,a were measured in plasma with radioimmunoassay. 15 ,ug/kg i.v. ofendotoxin induced no rise in pulmonary vascular resistance (PVR), but prevented AHPV so that the initial 33% (±2 SEM) decrease in perfusion to the hypoxic lung became only a 2% (± 1) decrease. Circulating levels of thromboxane and prostacyclin concurrently rose (P < 0.01) from nondetectable levels to 380 pg/ml (±40) and 360 pg/ml (±130). 150 ,g/kg of endotoxin induced a transient rise in PVR from 4.09 to 9.00 mm Hg/liter per min in association (r = 0.89, P < 0.01) with a sharp rise in thromboxane levels to 4,460 pg/ml (± 1,350) whereas prostacyclin levels were elevated less markedly to 550 pg/ml (+400). Prostaglandin F2<,X another vasoconstrictor, was not elevated. 30 min after endotoxin when PVR was again base line and AHPV lost, thromboxane fell significantly (P < 0.01) to 2,200 pg/ml (± 1,100) whereas prostacyclin remained elevated at 360 pg/ml (±135), a level similar to that seen when 15 ,g/kg of endotoxin induced Dr. Peterson is an Established Investigator ofthe American Heart Association.

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Regional edema formation in isolated perfused dog lungs.

Cited by 29 publications

References 10 publications

Computed tomography in adult respiratory distress syndrome: what has it taught us?

Computed tomography in adult respiratory distress syndrome: what has it taught us?

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

Role of Thromboxane and Prostacyclin in Pulmonary Vasomotor Changes after Endotoxin in Dogs

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