Acute Respiratory Distress Syndrome Secondary to Inhalation of Chlorine Gas in Sheep

Batchinsky, Andriy I.; Martini, David; Jordan, Bryan S.; Dick, Edward J.; Fudge, James Mack; Baird, Candace A; Hardin, Denise E; Cancio, Leopoldo C.

doi:10.1097/01.ta.0000205862.57701.48

Cited by 41 publications

(32 citation statements)

References 65 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In our first series of experiments, we exposed mice to Cl 2 at concentrations likely to be encountered in industrial accidents or deliberate release of Cl 2 into the atmosphere (19,26,27) and measured Na ϩ -dependent AFC in vivo at various times post exposure after the mice were returned to room air. Because our results indicated that exposure to Cl 2 decreased AFC, we performed additional studies in Xenopus oocytes injected with cRNAs of the human ENaC (hENaC) subunits (␣-, ␤-, and ␥-ENaC) to identify the cellular and molecular mechanisms by which HOCl (formed by the hydrolysis of Cl 2 gas) as well as reactive intermediates formed by the reaction of HOCl with components of the media decreased Na ϩ -and amiloride-sensitive currents (I Na and I amil , respectively).…”

mentioning

confidence: 99%

Inhibition of Lung Fluid Clearance and Epithelial Na+ Channels by Chlorine, Hypochlorous Acid, and Chloramines

Song¹,

Wei²,

Zhou³

et al. 2010

Journal of Biological Chemistry

View full text Add to dashboard Cite

We investigated the mechanisms by which chlorine (Cl 2 ) and its reactive byproducts inhibit Na ؉ -dependent alveolar fluid clearance (AFC) in vivo and the activity of amiloridesensitive epithelial Na ؉ channels (ENaC) by measuring AFC in mice exposed to Cl 2 (0 -500 ppm for 30 min) and Na ؉ and amiloride-sensitive currents (I Na and I amil , respectively) across Xenopus oocytes expressing human ␣-, ␤-, and ␥-ENaC incubated with HOCl (1-2000 M). Both Cl 2 and HOCl-derived products decreased AFC in mice and whole cell and single channel I Na in a dose-dependent manner; these effects were counteracted by serine proteases. Mass spectrometry analysis of the oocyte recording medium identified organic chloramines formed by the interaction of HOCl with HEPES (used as an extracellular buffer). In addition, chloramines formed by the interaction of HOCl with taurine or glycine decreased I Na in a similar fashion. Preincubation of oocytes with serine proteases prevented the decrease of I Na by HOCl, whereas perfusion of oocytes with a synthetic 51-mer peptide corresponding to the putative furin and plasmin cleaving segment in the ␥-ENaC subunit restored the ability of HOCl to inhibit I Na . Finally, I Na of oocytes expressing wild type ␣-and ␥-ENaC and a mutant form of ␤ENaC (S520K), known to result in ENaC channels locked in the open position, were not altered by HOCl. We concluded that HOCl and its reactive intermediates (such as organic chloramines) inhibit ENaC by affecting channel gating, which could be relieved by proteases cleavage.The balance of fluid covering the respiratory and alveolar epithelia is determined in part by the ability of these cells to transport sodium (Na ϩ ) and chloride (Cl Ϫ ) ions in a vectorial fashion. Active Na ϩ reabsorption across lung epithelia requires the coordinated entry of Na ϩ ions through cation-and Na ϩ -selective amiloride-sensitive channels (ENaC) 5 located at the apical membranes, their extrusion across the basolateral membranes by the electrogenic Na ϩ -K ϩ -ATPase, and the passive movement of K ϩ ions through basolateral K ϩ channels. The entry of Na ϩ ions through apical pathways is thought to be the rate-limiting step in this process (1-3). To preserve neutrality, Cl Ϫ ions follow Na ϩ ions both through transcellular and paracellular pathways (4, 5). The coordinated movement of Na ϩ and Cl Ϫ ions creates an oncotic gradient favoring the absorption of alveolar fluid.Injury to either apical or basolateral pathways by partially reduced intermediates may lead to impairment of fluid reabsorption, which in turn may result in pulmonary edema, hypoxemia, and eventually death from respiratory failure (6 -9). One such specie is hypochlorous acid (HOCl) 6 , which may be generated either endogenously or exogenously. Millimolar concentrations of HOCl may be generated by activated neutrophils and eosinophils by the catalytic actions of neutrophil-and eosinophil-derived myeloperoxidases on chloride (Cl Ϫ ) and hydrogen peroxide (H 2 O 2 ) in close proximity of the apical and basolatera...

show abstract

mentioning

confidence: 99%

Inhibition of Lung Fluid Clearance and Epithelial Na+ Channels by Chlorine, Hypochlorous Acid, and Chloramines

Song¹,

Wei²,

Zhou³

et al. 2010

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…3,9,12 There have been previous studies carried out with various doses and duration on chlorine gas in rats, sheep, porcine and dormice. 4,[13][14][15] We selected rats as the experiment animals in our study, since they met our conditions the best. Most of the recently reported chlorine gas exposures include exposures caused by the inhalation of toxic vapor arising from mixing of hypochlorite-containing household cleaning products with acid products.…”

Section: Resultsmentioning

confidence: 99%

“…15 During the follow-up, no deaths were seen in the Group treated with 120 ppm chlorine gas, while five out of 11 sheep had died in the group treated with 240-350 ppm, and 10 out of 12 sheep died in the group treated with 400-500 ppm chlorine gas. In the microscopic examination of the pulmonary tissues of the group treated with 120 ppm chlorine gas, they found localized regional necrosis associated with capillary congestion, edema, fibrin deposits and acute inflammation in the bronchial epithelium.…”

Section: Figurementioning

confidence: 99%

Histopathological Study of Short and Long-Term Pulmonary Effects of Nebulized Sodium Bicarbonate Treatment in Chlorine Gas Exposured Rats

Al¹,

Bozkurt²,

Yıldırım³

et al. 2010

Turkiye Klinikleri J Med Sci

View full text Add to dashboard Cite

A AB BS S T TR RA AC CT T O Ob bj je ec ct ti iv ve e: : So di um hypoch lo ri te (known as ble ach) and hydroch lo ric acid are tra di ti o nally used as cle a ning ma te ri als. Mix tu re of the se two li qu ids yi elds chlo ri ne gas. Chlo ri ne gas ex po su re is a fre qu ent re a son for emer gency con sul ta ti ons. The re is no ac cep ted spe ci fic tre at ment for re duc ti on of the pul mo nary in jury. In our study, we ha ve in ves ti ga ted his to pat ho lo gi cally the ef fect of ne bu lized so di um bi car bo na te, the use of which is al so con tro ver si al in the li te ra tu re, in the tre at ment of pulmo nary in jury ca u sed by chlo ri ne gas in ha la ti on. M Ma at te er ri ia al l a an nd d M Me et t h ho od ds s: : Forty-eight rats we re used. Rats we re ran domly dis tri bu ted in to five gro ups. Rats in Gro up 1 (n= 8) we re kept un tre a ted thro ugho ut the study. Rats in Gro up 2 (n= 8), Gro up 3 (n= 8), Gro up 4 (n= 12), and Gro up 5 (n= 12) we re expo sed to 155 ppm chlo ri ne gas in ha la ti on for five mi nu tes. Rats in Gro up 3 and 5 we re ad di ti o nally gi ven ne bu li zed so di um bi car bo na te fol lo wing chlo ri ne gas in ha la ti on. Rats in Gro up 2 and 3 we re sacri fi ced 30 mi nu tes af ter the chlo ri ne in ha la ti on, and rats in Gro up 4 and 5 we re sac ri fi ced 45 days after the in ha la ti on for his to pat ho lo gi cal exa mi na ti ons. Pul mo nary in jury gra de was determined and the re sults we re com pa red bet we en gro ups. Sta tis ti cal analy sis was performed using the SSPS 13.0 softwa re. R Re e s su ul lt ts s: : His to pat ho lo gi cal exa mi na ti on of the lungs of rats in Gro up 2 and 3 sho wed acu te injury. The re was no in jury in Gro up 1. All of the rats in Gro up 2 had Gra de 1 in jury. In Gro up 3, 50% of rats had Gra de 1 and 50% had Gra de 2 in juries. So me of the rats in Gro up 4 and Gro up 5 sho wed si mi lar in ters ti ti al fib ro sis and al ve o lar emph yse ma to us al te ra ti ons. Gra de 3 in jury was not de ter mined in any gro ups. C Co on nc c l lu u s si i o on n: : We conc lu ded that ne bu li zed so di um bi car bo na te in cre a ses the se verity of pul mo nary in jury in the short-term. It has no ef fects on the in jury in the long-term.K Ke ey y W Wo or rd ds s: : In ha la ti on ex po su re; so di um bi car bo na te Ö ÖZ ZE ET T A Am ma aç ç: : Halk ara sın da ça ma şır su yu ve tuz ru hu ola rak bi li nen sod yum hi pok lo rit ve hid rok lorik asit, ge le nek sel ola rak te miz lik ama cı ile kul la nı lır lar. Bu iki sı vı nın ka rış tı rıl ma sı so nu cu klor gazı or ta ya çı kar. Klor ga zı ze hir len me le ri acil ser vi se sık baş vu ru ne den le rin den bi ri si dir. Bu has ta la rın te da vi sin de ana yak la şım semp to ma tik ve des tek le yi ci te da vi dir. Or ta ya çı kan ak ci ğer ha sa rı nı azaltma ya yö ne lik ka bul gör müş spe si fik bir te da vi yak la şı mı yok tur. Ça lış ma mız da, klor ga zı in ha las yonu ile oluş tu ru lan ak ci ğer ha sa rı nın te da vi sin de, kul la nı mı li te ra tür de ...

show abstract

“…Based on the results of Yamamoto et al (17) and other previous reports (18)(19)(20), it has been suggested that there may be a latent period lasting up to 10 h and that symptoms may worsen 48 h following exposure to chlorine gas. In the current study, the patient developed respiratory failure after 4 h and symptoms worsened 13-14 h following initial exposure.…”

Section: Discussionmentioning

confidence: 99%

Bronchial damage and diffuse alveolar hemorrhage following chlorine gas inhalation: A case report

et al. 2017

View full text Add to dashboard Cite

Abstract. Chlorine is a toxic inhalant and sources of exposure for individuals include accidental releases of chlorine vapor due to industrial or chemical transportation accidents. Inhalation of a large quantity of gas may cause circulatory and respiratory disorders or even mortality; however, the effects of a small amount of chlorine gas may be asymptomatic. The present case study presents a successfully treated 55-year-old male patient exposed to chlorine gas, resulting in bronchial damage and diffuse alveolar hemorrhage. Endobronchial and alveolar injuries were evaluated by direct observation using fiberoptic bronchoscopy (FB) and analyzing bronchoalveolar lavage fluid obtained by FB. Taking a precise medical history from the patient is crucial to correctly diagnose toxic gas inhalation. In addition, a timely and proper evaluation with chest imaging as well as FB may provide useful clinical information. Therefore, clinicians should consider performing FB if the circumstances permit.

show abstract

Acute Respiratory Distress Syndrome Secondary to Inhalation of Chlorine Gas in Sheep

Abstract: Cl2 causes severe, dose-related lung injury, with features seen in both smoke inhalation and in ARDS secondary to systemic disease. This model will be used to test new therapeutic modalities.

Cited by 41 publications

References 65 publications

Inhibition of Lung Fluid Clearance and Epithelial Na+ Channels by Chlorine, Hypochlorous Acid, and Chloramines

Inhibition of Lung Fluid Clearance and Epithelial Na+ Channels by Chlorine, Hypochlorous Acid, and Chloramines

Histopathological Study of Short and Long-Term Pulmonary Effects of Nebulized Sodium Bicarbonate Treatment in Chlorine Gas Exposured Rats

Bronchial damage and diffuse alveolar hemorrhage following chlorine gas inhalation: A case report

Contact Info

Product

Resources

About