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Inhaled and intravenous corticosteroids both attenuate chlorine gas-induced lung injury in pigs
Östergötlands Läns Landsting, Centre for Teaching and Research in Disaster Medicine and Traumatology, Centre for Teaching and Research in Disaster Medicine and Traumatology. Linköping University, Faculty of Health Sciences.
Östergötlands Läns Landsting, Centre for Teaching and Research in Disaster Medicine and Traumatology, Centre for Teaching and Research in Disaster Medicine and Traumatology. Linköping University, Faculty of Health Sciences.
Östergötlands Läns Landsting, Centre for Teaching and Research in Disaster Medicine and Traumatology, Centre for Teaching and Research in Disaster Medicine and Traumatology. Linköping University, Faculty of Health Sciences.
Östergötlands Läns Landsting, Centre for Teaching and Research in Disaster Medicine and Traumatology, Centre for Teaching and Research in Disaster Medicine and Traumatology. Linköping University, Faculty of Health Sciences.
2005 (English)In: Acta Anaesthesiologica Scandinavica, ISSN 0001-5172, E-ISSN 1399-6576, Vol. 49, no 2, 183-190 p.Article in journal (Refereed) Published
Abstract [en]

Background:  The accidental release of chlorine gas is a constant threat in urban areas. The purpose of this randomized, blinded, controlled experiment was to examine the effects of post-injury administration of inhaled or intravenous corticosteroid in chlorine gas-injured pigs followed for 23 h.

Methods:  Anaesthetized, ventilated pigs (n = 24) in the prone position were exposed to chlorine gas (400 parts per million in air) (1160 mg/m3) for 15 min, then randomly allocated to receive inhaled budesonide (BUD) and intravenous placebo, intravenous betamethasone (BETA) and inhaled placebo or inhaled and intravenous placebo. Haemodynamics, gas exchange and lung mechanics were evaluated for 23 h after exposure to chlorine gas.

Results:  Airway and pulmonary artery pressures increased and arterial oxygenation fell sharply (from 13.5 ± 0.8 to 6.7 ± 0.9 kPa, P < 0.001) after chlorine gas exposure. These immediate changes were followed by a gradual improvement over 5–7 h to a stable level of dysfunction for the rest of the experiment in placebo animals. Arterial oxygen tension, pulmonary vascular resistance and airway pressure recovered faster and more completely in the budesonide and betamethasone groups than in the placebo group (P < 0.01). Lung wet weight to dry weight ratios were greater in the placebo group than in the budesonide and betamethasone groups (6.34 ± 0.59 vs. 5.56 ± 0.38 and 5.53 ± 0.54, respectively, P < 0.05). There was a trend towards lower histological injury scores compared with placebo in animals that received budesonide (P = 0.05) or betamethasone (P = 0.07).

Conclusion:  Treatment of chlorine gas lung injury with nebulized budesonide or intravenous betamethasone had similar positive effects on recovery of lung function.

Place, publisher, year, edition, pages
2005. Vol. 49, no 2, 183-190 p.
Keyword [en]
Acute lung injury, Chlorine gas, Experimental study, Intravenous corticosteroid, Nebulized corticosteroid, Randomized controlled study
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-45510DOI: 10.1111/j.1399-6576.2004.00563.xOAI: oai:DiVA.org:liu-45510DiVA: diva2:266406
Available from: 2009-10-11 Created: 2009-10-11 Last updated: 2012-10-26Bibliographically approved
In thesis
1. Pathophysiology and treatment of chlorine gas-induced lung injury: an experimental study in pigs
Open this publication in new window or tab >>Pathophysiology and treatment of chlorine gas-induced lung injury: an experimental study in pigs
2004 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

One of the most threatening scenarios in disaster medicine is the accidental release of toxic gases with the exposure of many people. In this respect, chlorine gas remains a significant threat due to its abundant use and transport through densely populated areas in modem society. Access to a simple and effective method of treatment that could be started early would be of great value. The main purpose of this study was to test a series of hypotheses related to chlorine gas lung injury and its treatment.

Anesthetized and mechanically ventilated pigs were exposed to chlorine gas (400 parts per million in air) using a closed system with a ventilator connected to gas cylinders. Plasma endothelin-1 (ET -1) and pro inflammatory cytokines were evaluated for 5 hours after injury while hemodynamics, gas exchange and lung mechanics were followed for 23 hours. Histopathology and lung water balance were assessed at the end of the experiment.

Chlorine gas exposure induced a rise in circulating ET-1 and circulating cytokines (TNF-α, and IL-1ß, IL-6). Pretreatment or treatment with tezosentan, a potent dual endothelin receptor antagonist, reduced the deterioration of pulmonary function induced by chlorine gas inhalation. Immediate prone positioning after chlorine gas injury not only inhibited deterioration of gas exchange but was also associated with improved pulmonary function and oxygen transport. Nebulized budesonide given within 30 minutes after chlorine gas lung injury was effective in preventing further progression of lung dysfunction but the effect of treatment given beyond 60 minutes was less efficient. The positive effects on pulmonary function and lung water were similar whether corticosteroids were given by aerosol or intravenously. Combined treatment with nebulized terbutaline and budesonide was associated with better recovery of lung function than either drug alone.

In conclusion, these studies outline the early pathophysiology of chlorine gas injury. They show that the endothelin system mediates the early pulmonary hypertensive and also to some extent the brochoconstrictive responses to inhaled chlorine gas. The work supports early administration of corticosteroids and ß2-agonists for individuals that are exposure to chlorine gas. In addition, early prone positioning of patients with severe chlorine gas lung injury may be useful.

Place, publisher, year, edition, pages
Linköping: Linköpings universitet, 2004. 53 p.
Series
Linköping University Medical Dissertations, ISSN 0345-0082 ; 877
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-24066 (URN)3625 (Local ID)91-7373-853-0 (ISBN)3625 (Archive number)3625 (OAI)
Public defence
2004-12-20, Aulan, Katastrofmedicinskt Centrum, Hälsouniversitetet, Linköping, 13:00 (Swedish)
Opponent
Available from: 2009-10-07 Created: 2009-10-07 Last updated: 2012-10-26Bibliographically approved

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Wang, JianpuEdston, ErikWalther, Sten

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