Adult ; Chlorine ; poisoning ; Humans ; Male ; Middle Aged ; Phosgene ; poisoning ; Respiratory Distress Syndrome, Adult ; chemically induced

OBJECTIVETo analysis clinical characteristics of the multiple organ dysfunction syndrome (MODS) caused by acute paraquat poisoning (APP).

METHODClinical data of 68 APP cases from Jan 2006 to Jun 2009, including age, gender, poisoning time and dosage, and MODS time, were compared in two groups, i.e. the death (37 cases) and survived (31cases) groups. It was less than 24 hours from poisoning to rescue in all cases.

RESULTSAmong the 68 cases, the incident rate of ARDS was 51.47% (35 cases). The rate of acute lung injure was 97.1% (66 cases). The mortality was 54.4% (37 cases). There was no significant difference in age and gender between both groups (P > 0.05). The dosages and times from poisoning to rescue were significant different between two groups (P < 0.05, P < 0.01). In the death group, proportion of amounts (> 3) of organs related with MODS was 70.29%, which was significantly higher than that (38.71%) in survived group (P < 0.01). MODS and ALI/ARDS occurred in death group earlier than those in survival group (P < 0.05). On the other hand, cardiac, hepatic and renal damage occurred earlier than the lung injure.

CONCLUSIONMODS in APP patients occurred earlier, were more sever, and caused higher mortality. The poisoning dosage and time were important prognostic factors.

Adult ; Female ; Humans ; Male ; Middle Aged ; Multiple Organ Failure ; chemically induced ; diagnosis ; Paraquat ; poisoning ; Prognosis ; Respiratory Distress Syndrome, Adult ; chemically induced ; diagnosis ; Retrospective Studies ; Young Adult

Animals ; Male ; Particle Size ; Rats ; Rats, Sprague-Dawley ; Respiratory Distress Syndrome, Adult ; chemically induced ; Silicon Dioxide ; chemistry ; toxicity

Antithymocyte globulin (ATG) has long been used for immune-induction and anti-rejection treatments for solid organ transplantations. To date, few cases of ATG-induced acute respiratory distress syndrome (ARDS) have been published. Here, we present a case of ARDS caused by a single low-dose of ATG in a renal transplant recipient and the subsequent treatments administered. Although the patient suffered from ARDS and delayed graft function, he was successfully treated. We emphasize that the presence of such complications should be considered when unexplained respiratory distress occurs. Early use of corticosteroids, adjustment of immunosuppressive regimens, and conservative fluid management, as well as empiric antimicrobial therapies, may be effective strategies for the treatment of ARDS caused by ATG.
Adrenal Cortex Hormones ; therapeutic use ; Adult ; Antilymphocyte Serum ; adverse effects ; Humans ; Kidney Transplantation ; Male ; Respiratory Distress Syndrome, Adult ; chemically induced ; drug therapy

The expression of intercellular adhesion molecule-1 (ICAM-1) in the pathogenesis of heroin-induced acute lung injury (ALI) in rats was investigated. The model of ALI was established by intravenous injection of heroin into tail vein in rats. Thirty-six rats were randomly divided into heroin-treated groups (1 h, 2 h, 4 h, 6 h and 24 h) and normal control group. Changes in histopathologic morphology and biological markers of ALI were measured. The expression of ICAM-1 in lung tissue was detected by using immunohistochemistry and RT-PCR. The results showed that the W/D ratio and protein contents in BALF of the heroin-treated groups were significantly higher than that of the, control group (P<0.01). The histopathological changes in the lung tissue were more obvious in heroin-treated groups. The ICAM-1 protein and mRNA expression in the lung tissue of heroin-treated groups were significantly increased as compared with that of the control group (P<0.01), and correlated with the ALI parameters in a time-dependent manner. Increasing of ICAM-1 expression was involved in the formation of heroin-induced lung injury. Furthermore, the level of expression was positively correlated with the severity of lung injury.
Animals ; Heroin ; Intercellular Adhesion Molecule-1 ; biosynthesis ; genetics ; Male ; RNA, Messenger ; biosynthesis ; genetics ; Random Allocation ; Rats ; Rats, Wistar ; Respiratory Distress Syndrome, Adult ; chemically induced ; metabolism ; pathology

The aim of this study was to determine the role of neutrophil collagenase in the pathogenesis of acute lung injury induced by endotoxin. 28 Sprague-Dawley were randomized into control group and LPS-enduced groups. Samples of left lung were obtained in 2 h (group L1), 6 h (group L2), 12 h (group L3) after intravenous LPS. Immunohistochemsitry was employed for detection of expression of neutrophil collagenase. Pathological scores, lung wet/dry weight ratio and the number of neutrophils were measured. The results showed that the concentration of neutrophil collagenase in LPS-enduced groups (group L1, L2, L3) were significantly higher than that of control group (P<0.01). Pathological scores, lung wet/dry weight ratio and the number of neutrophils in LPS-enduced groups (group L1, L2, L3) were also significantly higher than that of control group (P<0.01). Moreover, among group L1, L2 and L3, there were significant correlations in concentration of neutrophil collagenase and pathological scores, lung wet/dry weight ratio, the number of neutrophils (P<0.05). The present study showed that neutrophil collagenase play an important role in the pathogenesis and progress of endotoxic acute lung injury.
Animals ; Endotoxins ; Female ; Lung ; pathology ; Male ; Matrix Metalloproteinase 8 ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Respiratory Distress Syndrome, Adult ; chemically induced ; enzymology ; etiology ; pathology

OBJECTIVEAlveolar type II (AT II) cells play a crucial role in the maintenance of pulmonary surfactant homeostasis and pulmonary immunity. The effects of dexamethasone (Dex) on the ultrastructure of AT II cells after acute lung injury remain unknown. This study focused on the ultrastructural changes caused by acute lung injury and on the effects of Dex administration on these ultrastructural changes in young rats.

METHODSSeventy-two 21-day-old Sprague-Dawley rats were randomly divided into control, acute lung injury and Dex-treated groups. Rats in the lung injury group were intraperitoneally injected with 4 mg/kg lipopolysaccharide (LPS) in order to induce acute lung injury, while the control rats were injected with the same amount of normal saline (NS). The Dex-treated group was injected first with LPS followed 1 hr later by Dex (5 mg/kg) injection. Eight rats in each group were sacrificed 24, 48 and 72 hrs after LPS or NS injection. Lung samples were obtained from the lower parts of left lungs and fixed with 2.5% glutaraldehyde for transmission electron microscope examination.

RESULTSMicrovilli of AT II cells disappeared and the number of lamellar bodies (LBs) increased in the lung injury group 24 hrs after LPS injection. The ring-like arrangement of LBs around nuclei was present until 48 hrs after LPS injection. By 48 hrs after LPS injection, giant LBs with vacuole-like abnormalities appeared. The shape of nuclei became irregular and the border of the nuclei became blurred. By 72 hrs after LPS injection, the number of LBs was obviously reduced; nucleoli disappeared; and karyolysis occurred in some of the nuclei. In contrast, in the Dex-treated group, LBs crowded on one side of AT II cells and exocytosis appeared on the same side by 24 hrs after LPS injection. By 48 hrs, the number of LBs was reduced. The number of mitochondria increased, and some of them became swollen and enlarged. However, by 72 hrs, the number of LBs increased and the ring-like arrangement of LBs around the nucleus again appeared.

CONCLUSIONSUltrastructural changes of AT II cells following lung injury induced by LPS were time-dependent in young rats. Dex may ameliorate AT II cell injury and promote functional restoration of AT II cells in LPS-induced acute lung injury.

Animals ; Dexamethasone ; pharmacology ; therapeutic use ; Lipopolysaccharides ; toxicity ; Pulmonary Alveoli ; drug effects ; ultrastructure ; Rats ; Rats, Sprague-Dawley ; Respiratory Distress Syndrome, Adult ; chemically induced ; drug therapy ; pathology

OBJECTIVEImpaired active fluid transport of alveolar epithelium may involve in the pathogenesis and resolution of alveolar edema. The objective of this study was to explore the changes in alveolar epithelial liquid clearance during lung edema following acute lung injury induced by oleic acid.

METHODSForty-eight Wistar rats were randomly divided into six groups, i.e., injured, amiloride, ouabain, amiloride plus ouabain and terbutaline groups. Twenty-four hours after the induction of acute lung injury by intravenous oleic acid (0.25 ml/kg), 5% albumin solution with 1.5 microCi (125)I-labeled albumin (5 ml/kg) was delivered into both lungs via trachea. Alveolar liquid clearance (ALC), extravascular lung water (EVLW) content and arterial blood gases were measured one hour thereafter.

RESULTSAt 24 h after the infusion of oleic acid, the rats developed pulmonary edema and severe hypoxemia, with EVLW increased by 47.9% and ALC decreased by 49.2%. Addition of either 2x10(-3) M amiloride or 5x10(-4) M ouabain to the instillation further reduced ALC and increased EVLW. ALC increased by approximately 63.7% and EVLW decreased by 46.9% with improved hypoxemia in the Terbutaline (10(-4) M) group, compared those in injured rats. A significant negative correlation was found between the increment of EVLW and the reduction of ALC.

CONCLUSIONSActive fluid transport of alveolar epithelium might play a role in the pathogenesis of lung edema in acute lung injury.

Adrenergic beta-Agonists ; pharmacology ; Animals ; Epithelium ; metabolism ; Oleic Acid ; adverse effects ; Pulmonary Alveoli ; metabolism ; Random Allocation ; Rats ; Rats, Wistar ; Respiratory Distress Syndrome, Adult ; chemically induced ; metabolism ; Terbutaline ; pharmacology

OBJECTIVETo investigate whether acute lung injury (ALI) and changes of myocardial ATP enzymes were induced by intravenous or intraventricle of left heart injection of lipopolysaccharide (LPS) in aging rats.

METHODS40 male Wistar rats were used for reproducing aging animal model. Aging rats were randomly divided into aging control group (n = 8), ALI group (LPS, 5 mg/kg body weight intravenous injection, n = 16), and LPS group (same dosage LPS, intraventricle of left heart injection, n = 16). The samples (blood, lung and heart) were collected at 2, 6 hours after LPS or saline administration.

RESULTSCompared with aging control, protein content in bronchial alveolar lavage fluid (BALF), ratio of lung wet/dry weight and the LA, NO2-/NO3- and MDA contents in blood were increased markedly (P < 0.01) at 2, 6 hours in ALI group. The GSH-Px, Na(+)-K(+)-ATPase activities in lung tissue were decreased significantly (P < 0.01), but NO2-/NO3- content in lung tissue was increased obviously (P < 0.01) at 2 hours in ALI group. These changes were maintained until at 6 hours after LPS administration. The above parameters were no obviously changes in myocardium at 2 hours after LPS administration in ALI group. But at 6 hours, MDA content was increased obviously (P < 0.01); Na(+)-K(+)-ATPase, Ca(2+)-Mg(2+)-ATPase and GSH-Px activities in myocardium were decreased markedly (P < 0.01). While in LPS group, only NO2-/NO3- contents were increased (P < 0.05) in blood and lung tissue as well as Na(+)-K(+)-ATPase activity in lung tissue were decreased (P < 0.05), another parameters had no obvious changes.

CONCLUSIONSALI was obviously formed by intravenous injection LPS after 2, 6 hours in aging rats. Myocardial enzyme etc decreased only at 6 hours in ALI group. But above parameters were no obviously changes in LPS group. It was suggested that there was probable myocardial damage in rats of ALI group, and it was mainly induced by ALI.

Aging ; Animals ; Glutathione Peroxidase ; metabolism ; Lipopolysaccharides ; Male ; Myocardium ; enzymology ; Rats ; Rats, Wistar ; Respiratory Distress Syndrome, Adult ; chemically induced ; enzymology ; Sodium-Potassium-Exchanging ATPase ; metabolism

ObjectiveExposure to halogens, such as chlorine or bromine, results in environmental and occupational hazard to the lung and other organs. Chlorine is highly toxic by inhalation, leading to dyspnea, hypoxemia, airway obstruction, pneumonitis, pulmonary edema, and acute respiratory distress syndrome (ARDS). Although bromine is less reactive and oxidative than chlorine, inhalation also results in bronchospasm, airway hyperresponsiveness, ARDS, and even death. Both halogens have been shown to damage the systemic circulation and result in cardiac injury as well. There is no specific antidote for these injuries since the mechanisms are largely unknown.

Data SourcesThis review was based on articles published in PubMed databases up to January, 2018, with the following keywords: "chlorine," "bromine," "lung injury," and "ARDS."

Study SelectionThe original articles and reviews including the topics were the primary references.

ResultsBased on animal studies, it is found that inhaled chlorine will form chlorine-derived oxidative products that mediate postexposure toxicity; thus, potential treatments will target the oxidative stress and inflammation induced by chlorine. Antioxidants, cAMP-elevating agents, anti-inflammatory agents, nitric oxide-modulating agents, and high-molecular-weight hyaluronan have shown promising effects in treating acute chlorine injury. Elevated free heme level is involved in acute lung injury caused by bromine inhalation. Hemopexin, a heme-scavenging protein, when administered postexposure, decreases lung injury and improves survival.

ConclusionsAt present, there is an urgent need for additional research to develop specific therapies that target the basic mechanisms by which halogens damage the lungs and systemic organs.

Acute Lung Injury ; chemically induced ; Animals ; Chlorine ; toxicity ; Halogens ; toxicity ; Humans ; Lung ; drug effects ; pathology ; Respiratory Distress Syndrome, Adult ; drug therapy