High-dose heparin fails to improve acute lung injury following smoke inhalation in sheep

2003 ◽  
Vol 104 (4) ◽  
pp. 349-356 ◽  
Author(s):  
Kazunori MURAKAMI ◽  
Perenlei ENKHBAATAR ◽  
Katsumi SHIMODA ◽  
Akio MIZUTANI ◽  
Robert A. COX ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Responses ◽  
Inhalation Injury ◽  
Smoke Inhalation ◽  
High Dose ◽  
Heparin Infusion ◽  
Infusion Group ◽  
Dose Heparin ◽  
Lung Dysfunction

Thrombin is involved in various inflammatory responses. In sepsis, coagulation abnormalities are major complications. Acute lung injury is one of the most life-threatening problems that can result from sepsis. We hypothesized that high-dose heparin might be effective in attenuating acute lung injury in our sepsis model. Female sheep (n = 16) were surgically prepared for the study. After a tracheotomy, 48 breaths of cotton smoke (<40°C) were insufflated into the airway. Afterwards, live Pseudomonas aeruginosa (5×1011 colony-forming units) bacteria were instilled into the lung. All sheep were ventilated mechanically with 100% O2, and were divided into three groups: a heparin infusion group (n = 6), a Ringer's lactate infusion group (n = 6), and a sham-injury group (n = 4; surgically prepared in the same fashion but receiving no inhalation injury or bacteria). The treatment was started 1h after the insult, and was continued thereafter for 24h. The dose of heparin was adjusted by monitoring to target an activated clotting time of between 300 and 400s (baseline = approx. 150s). Sheep exposed to lung injury presented with typical hyperdynamic cardiovascular changes, including an increased cardiac output and a fall in systemic vascular resistance. There was a decrease in the arterial partial pressure of O2. In conclusion, high-dose heparin did not prevent lung dysfunction in this model, in which acute lung injury was induced by combined smoke and septic challenge.

High-dose heparin fails to improve acute lung injury following smoke inhalation in sheep

2003 ◽  
Vol 104 (4) ◽  
pp. 349 ◽  
Author(s):  
Kazunori MURAKAMI ◽  
Perenlei ENKHBAATAR ◽  
Katsumi SHIMODA ◽  
Akio MIZUTANI ◽  
Robert A. COX ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Smoke Inhalation ◽  
High Dose ◽  
Dose Heparin

scholarly journals The HMGB1-RAGE axis mediates traumatic brain injury–induced pulmonary dysfunction in lung transplantation

2014 ◽  
Vol 6 (252) ◽  
pp. 252ra124-252ra124 ◽  
Author(s):  
Daniel J. Weber ◽  
Adam S. A. Gracon ◽  
Matthew S. Ripsch ◽  
Amanda J. Fisher ◽  
Bo M. Cheon ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Acute Lung Injury ◽  
Brain Injury ◽  
Lung Injury ◽  
Lung Transplantation ◽  
Inflammatory Responses ◽  
Pulmonary Dysfunction ◽  
Wild Type ◽  
Hmgb1 Protein ◽  
Lung Dysfunction

Traumatic brain injury (TBI) results in systemic inflammatory responses that affect the lung. This is especially critical in the setting of lung transplantation, where more than half of donor allografts are obtained postmortem from individuals with TBI. The mechanism by which TBI causes pulmonary dysfunction remains unclear but may involve the interaction of high-mobility group box-1 (HMGB1) protein with the receptor for advanced glycation end products (RAGE). To investigate the role of HMGB1 and RAGE in TBI-induced lung dysfunction, RAGE-sufficient (wild-type) or RAGE-deficient (RAGE−/−) C57BL/6 mice were subjected to TBI through controlled cortical impact and studied for cardiopulmonary injury. Compared to control animals, TBI induced systemic hypoxia, acute lung injury, pulmonary neutrophilia, and decreased compliance (a measure of the lungs’ ability to expand), all of which were attenuated in RAGE−/−mice. Neutralizing systemic HMGB1 induced by TBI reversed hypoxia and improved lung compliance. Compared to wild-type donors, lungs from RAGE−/−TBI donors did not develop acute lung injury after transplantation. In a study of clinical transplantation, elevated systemic HMGB1 in donors correlated with impaired systemic oxygenation of the donor lung before transplantation and predicted impaired oxygenation after transplantation. These data suggest that the HMGB1-RAGE axis plays a role in the mechanism by which TBI induces lung dysfunction and that targeting this pathway before transplant may improve recipient outcomes after lung transplantation.

scholarly journals Dynamic Tracking Human Mesenchymal Stem Cells Tropism following Smoke Inhalation Injury in NOD/SCID Mice

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
MeiJuan Song ◽  
Qi Lv ◽  
XiuWei Zhang ◽  
Juan Cao ◽  
ShuLi Sun ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Inhalation Injury ◽  
Scid Mice ◽  
Alveolar Epithelial Cells ◽  
Smoke Inhalation ◽  
Control Group ◽  
Smoke Inhalation Injury

Multiple preclinical evidences have supported the potential value of mesenchymal stem cells (MSCs) for treatment of acute lung injury (ALI). However, few studies focus on the dynamic tropism of MSCs in animals with acute lung injury. In this study, we track systemically transplanted human bone marrow-derived mesenchymal stem cells (hBMSCs) in NOD/SCID mice with smoke inhalation injury (SII) through bioluminescence imaging (BLI). The results showed that hBMSCs systemically delivered into healthy NOD/SCID mouse initially reside in the lungs and then partially translocate to the abdomen after 24 h. Compared with the uninjured control group treated with hBMSCs, higher numbers of hBMSCs were found in the lungs of the SII NOD/SCID mice. In both the uninjured and SII mice, the BLI signals in the lungs steadily decreased over time and disappeared by 5 days after treatment. hBMSCs significantly attenuated lung injury, elevated the levels of KGF, decreased the levels of TNF-αin BALF, and inhibited inflammatory cell infiltration in the mice with SII. In conclusion, our findings demonstrated that more systemically infused hBMSCs localized to the lungs in mice with SII. hBMSC xenografts repaired smoke inhalation-induced lung injury in mice. This repair was maybe due to the effect of anti-inflammatory and secreting KGF of hMSCs but not associated with the differentiation of the hBMSCs into alveolar epithelial cells.

scholarly journals Vitamin E attenuates acute lung injury in sheep with burn and smoke inhalation injury

Redox Report ◽  
2006 ◽  
Vol 11 (2) ◽  
pp. 61-70 ◽  
Author(s):  
Naoki Morita ◽  
Katsumi Shimoda ◽  
Maret G. Traber ◽  
Martin Westphal ◽  
Perenlei Enkhbaatar ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Vitamin E ◽  
Lung Injury ◽  
Inhalation Injury ◽  
Smoke Inhalation ◽  
Smoke Inhalation Injury

Influence of Nebulized Unfractionated Heparin and N-Acetylcysteine in Acute Lung Injury After Smoke Inhalation Injury

2009 ◽  
Vol 30 (2) ◽  
pp. 249-256 ◽  
Author(s):  
Andrew C. Miller ◽  
Abel Rivero ◽  
Sophia Ziad ◽  
David J. Smith ◽  
Elamin M. Elamin
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Unfractionated Heparin ◽  
Inhalation Injury ◽  
Smoke Inhalation ◽  
Smoke Inhalation Injury

scholarly journals There is no fire without smoke! Pathophysiology and treatment of inhalational injury in burns: A narrative review

2020 ◽  
Vol 48 (2) ◽  
pp. 114-122
Author(s):  
Anthony D Holley ◽  
Michael C Reade ◽  
Jeffrey Lipman ◽  
Jeremy Cohen
Keyword(s):  
Critical Care ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Inhalation Injury ◽  
Morbidity And Mortality ◽  
Smoke Inhalation ◽  
Novel Therapies ◽  
Management Implications ◽  
Severe Burns ◽  
Inhalational Injury

Smoke inhalation resulting in acute lung injury is a common challenge facing critical care practitioners caring for patients with severe burns, contributing significantly to morbidity and mortality. The intention of this review is to critically evaluate the published literature and trends in the diagnosis, management, implications and novel therapies in caring for patients with inhalation injury.

Pathophysiology of acute lung injury in combined burn and smoke inhalation injury

2004 ◽  
Vol 107 (2) ◽  
pp. 137-143 ◽  
Author(s):  
Perenlei ENKHBAATAR ◽  
Daniel L. TRABER
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Burn Injury ◽  
Surgical Excision ◽  
Inhalation Injury ◽  
Burn Injuries ◽  
Morbidity And Mortality ◽  
Smoke Inhalation ◽  
Therapeutic Approaches ◽  
Smoke Inhalation Injury

In the U.S.A., more than 1 million burn injuries occur every year. Although the survival from burn injury has increased in recent years with the development of effective fluid resuscitation management and early surgical excision of burned tissue, the mortality of burn injury is still high. In these fire victims, progressive pulmonary failure and cardiovascular dysfunction are important determinants of morbidity and mortality. The morbidity and mortality increases when burn injury is associated with smoke inhalation. In the present review, we will describe the pathophysiological aspects of acute lung injury induced by combined burn and smoke inhalation and examine various therapeutic approaches.

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