Lung edema formation following inhalation injury: role of the bronchial blood flow

Abdi, Salahadin; Herndon, David N.; Traber, Lillian D.; Ashley, K. D.; Stothert, Joseph C.; Maguire, J.; Butler, Robert S.; Traber, Daniel L.

doi:10.1152/jappl.1991.71.2.727

Cited by 46 publications

(32 citation statements)

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“…Magno and Fishman (10) showed that the tracheal bronchial artery is one of the major sources of blood to the lung. We have also reported that occlusion of the bronchial artery prevented the increase in pulmonary transvascular fluid flux seen with inhalation injury (3,12). These findings were recently confirmed by others (7).…”

Section: Discussionsupporting

confidence: 84%

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Role of anti-L-selectin antibody in burn and smoke inhalation injury in sheep

Katahira¹,

Murakami²,

Schmalstieg

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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We hypothesized that the antibody neutralization of L-selectin would decrease the pulmonary abnormalities characteristic of burn and smoke inhalation injury. Three groups of sheep ( n = 18) were prepared and randomized: the LAM-(1–3) group ( n = 6) was injected intravenously with 1 mg/kg of leukocyte adhesion molecule (LAM)-(1-3) (mouse monoclonal antibody against L-selectin) 1 h after the injury, the control group ( n = 6) was not injured or treated, and the nontreatment group ( n = 6) was injured but not treated. All animals were mechanically ventilated during the 48-h experimental period. The ratio of arterial Po 2 to inspired O2 fraction decreased in the LAM-(1–3) and nontreatment groups. Lung lymph flow and pulmonary microvascular permeability were elevated after injury. This elevation was significantly reduced when LAM-(1–3) was administered 1 h after injury. Nitrate/nitrite (NO x ) amounts in plasma and lung lymph increased significantly after the combined injury. These changes were attenuated by posttreatment with LAM-(1–3). These results suggest that the changes in pulmonary transvascular fluid flux result from injury of lung endothelium by polymorphonuclear leukocytes. In conclusion, posttreatment with the antibody for L-selectin improved lung lymph flow and permeability index. L-selectin appears to be principally involved in the increased pulmonary transvascular fluid flux observed with burn/smoke insult. L-selectin may be a useful target in the treatment of acute lung injury after burn and smoke inhalation.

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Section: Discussionsupporting

confidence: 84%

“…Hemodynamic variables and blood gases were obtained at 3,6,12,18,24,30,36,42, and 48 h after injury in all groups.…”

Section: Methodsmentioning

confidence: 99%

Role of anti-L-selectin antibody in burn and smoke inhalation injury in sheep

Katahira¹,

Murakami²,

Schmalstieg

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…This statement is supported by the results of three independent methods: the decrease in lung tissue myeloperoxidase activity, an index of neutrophil accumulation (21); the lower histological scores for alveolar as well as interstitial neutrophils; and the reduced number of neutrophils in the lung lymph. Neutrophil adherence to the endothelium can directly induce endothelial injury resulting in vascular leakage and eventually pulmonary edema (22, 23). The clinical relevance of neutrophils in the pathogenesis of inhalation injury was confirmed by Basadre et al (24), who demonstrated that in leukocyte-depleted sheep the characteristic changes, such as a fall in PaO2/FIO2 ratio and an increase in MPAP and transvascular fluid flux, were markedly attenuated.…”

Section: Discussionmentioning

confidence: 99%

Antithrombin Attenuates Vascular Leakage via Inhibiting Neutrophil Activation in Acute Lung Injury

Rehberg

Yamamoto

Sousse

et al. 2013

Critical Care Medicine

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Objective To test the hypothesis that restoration of antithrombin plasma concentrations attenuates vascular leakage by inhibiting neutrophil activation through syndecan-4 receptor inhibition in an established ovine model of acute lung injury. Design Randomized controlled laboratory experiment. Setting University animal research facility. Subjects Eighteen chronically instrumented sheep. Interventions Following combined burn and smoke inhalation injury (40% of total body surface area, third-degree flame burn; 4 × 12 breaths of cold cotton smoke), chronically instrumented sheep were randomly assigned to receive an IV infusion of 6 IU/kg/hr recombinant human antithrombin III or normal saline (n = 6 each) during the 48-hour study period. In addition, six sham animals (not injured, continuous infusion of vehicle) were used to obtain reference values for histological and immunohistochemical analyses. Measurements and Main Results Compared to control animals, recombinant human antithrombin III reduced the number of neutrophils per hour in the pulmonary lymph (p < 0.01 at 24 and 48 hr), alveolar neutrophil infiltration (p = 0.04), and pulmonary myeloperoxidase activity (p = 0.026). Flow cytometric analysis revealed a significant reduction of syndecan-4-positive neutrophils (p = 0.002 vs control at 24 hr). Treatment with recombinant human antithrombin III resulted in a reduction of pulmonary nitrosative stress (p = 0.002), airway obstruction (bronchi: p = 0.001, bronchioli: p = 0.013), parenchymal edema (p = 0.044), and lung bloodless wet-to-dry-weight ratio (p = 0.015). Clinically, recombinant human antithrombin III attenuated the increased pulmonary transvascular fluid flux (12–48 hr: p ≤ 0.001 vs control each) and the deteriorated pulmonary gas exchange (12–48 hr: p < 0.05 vs control each) without increasing the risk of bleeding. Conclusions The present study provides evidence for the interaction between antithrombin and neutrophils in vivo, its pathophysiological role in vascular leakage, and the therapeutic potential of recombinant human antithrombin III in a large animal model of acute lung injury.

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“…Previous investigators have shown that the flow of lymph from a sheep leg fistula goes up after smoke inhalation combined with burn (Lalonde et al, 1992). We and others have also shown that the bronchial arteries play a major role in smoke-induced pulmonary edema perhaps by carrying mediators of inflammation from the severely injured proximal airway to the lung parenchyma (Hales et al, 1989;Adbi et al, 1991;Efimova et al, 2000).…”

Section: Introductionmentioning

confidence: 75%