Acute Disease ; Cytokines ; metabolism ; Lung Injury ; chemically induced ; Paraquat ; toxicity

Acute Lung Injury/chemically induced* ; Animals ; Bronchoalveolar Lavage Fluid ; Lipopolysaccharides ; Lung ; Mice ; Mice, Inbred C57BL

Acute Lung Injury ; chemically induced ; pathology ; Animals ; Humans ; Lung ; pathology ; Nanospheres ; adverse effects ; Titanium ; adverse effects

Accidents ; Acute Lung Injury ; chemically induced ; Administration, Oral ; Humans ; Mediastinal Emphysema ; complications ; Potassium Permanganate ; toxicity

Ingestion of corrosive substances can severely burn the upper digestive tract leading to bleeding or perforation, and may even be life-threatening. Less commonly, damage to the trachea and bronchi is involved. In this paper, a case of corrosive digestive tract injury and lung injury after oral administration of pipeline dredging agent (the main components are hydroxide, sodium carbonate, sodium hypochlorite, etc.) was analyzed. After active rescue treatment, the patient died of massive hemoptysis. It is suggested that serious complications may occur after ingestion of corrosive substances. Timely diagnosis and reasonable medical management are needed to improve the level of recognition and treatment of such diseases.
Humans ; Caustics ; Lung Injury/chemically induced* ; Gastrointestinal Tract ; Burns, Chemical/therapy* ; Eating

BACKGROUNDOrganophosphate poisoning is an important health problem in developing countries which causes death mainly by inducing acute lung injury. In this study, we examined the effects of penehyclidine hydrochloride (PHC), a selective M-receptor inhibitor, on dichlorvos-induced acute lung injury in swine.

METHODSTwenty-two female swines were randomly divided into control (n = 5), dichlorvos (n = 6), atropine (n = 6), and PHC (n = 5) groups. Hemodynamic data, extravascular lung water index (EVLWI), and pulmonary vascular permeability index (PVPI) were monitored; blood gas analysis and acetylcholinesterase (AchE) levels were measured. PaO2/FiO2, cardiac index (CI), and pulmonary vascular resistance indices (PVRI) were calculated. At termination of the study, pulmonary tissue was collected for ATPase activity determination and wet to dry weight ratio (W/D) testing 6 hours post-poisoning. TUNEL assay, and Bax, Bcl-2, and caspase-3 expression were applied to pulmonary tissue, and histopathology was observed.

RESULTSAfter poisoning, PHC markedly decreased PVRI, increased CI more effectively than atropine. Anticholinergic treatment reduced W/D, apoptosis index (AI), and mitigated injury to the structure of lung; however, PHC reduced AI and caspase-3 expression and improved Bcl-2/Bax more effectively than atropine. Atropine and PHC improved ATPase activities; a significant difference between groups was observed in Ca(2+)-ATPase activity, but not Na(+)-K(+)-ATPase activity.

CONCLUSIONSThe PHC group showed mild impairment in pathology, less apoptotic cells, and little impact on cardiac function compared with the atropine group in dichlorvos-induced acute lung injury.

Acute Lung Injury ; chemically induced ; drug therapy ; Animals ; Dichlorvos ; toxicity ; Female ; Quinuclidines ; therapeutic use ; Swine

BACKGROUNDYoung children are susceptible to pulmonary injury, and acute lung injury (ALI) often results in a high mortality and financial costs in pediatric patients. A good ALI model will help us to gain a better understanding of the real pathophysiological picture and to evaluate novel treatment approaches to acute respiratory distress syndrome (ARDS) more accurately and liberally. This study aimed to establish a hemodynamically stable and reproducible model with ALI in piglet induced by oleic acid.

METHODSSix Chinese mini-piglets were used to establish ALI models by oleic acid. Hemodynamic and pulmonary function data were measured. Histopathological assessment was performed.

RESULTSMean blood pressure, heart rate (HR), cardiac output (CO), central venous pressure (CVP) and left atrial pressure (LAP) were sharply decreased after oleic acid given, while the mean pulmonary arterial pressure (MPAP) was increased in comparison with baseline (P < 0.05). pH, arterial partial pressure of O2 (PaO2), PaO2/inspired O2 fraction (FiO2) and lung compliance decreased, while PaCO2 and airway pressure increased in comparison with baseline (P < 0.05). The lung histology showed severe inflammation, hyaline membranes, intra-alveolar and interstitial hemorrhage.

CONCLUSIONThis experiment established a stable model which allows for a diversity of studies on early lung injury.

Acute Lung Injury ; chemically induced ; Animals ; Disease Models, Animal ; Female ; Male ; Oleic Acid ; toxicity ; Swine

BACKGROUNDPediatric patients are susceptible to lung injury that does not respond to traditional therapies. Partial liquid ventilation (PLV) has been developed as an alternative ventilatory strategy for treating severe lung injury. The aim of this study is to investigate the effect of PLV on lung function in immature piglets.

METHODSAcute lung injury was induced in 12 Chinese immature piglets by oleic acid (OA). The animals were randomly assigned to two groups (n = 6 each group): (1) conventional mechanical ventilation (MV) group and (2) PLV with FC-77 (10 ml/kg) group. Mean arterial blood pressure (MAP), mean pulmonary arterial pressure (MPAP), central venous pressure (CVP), left atrial pressure (LAP), systemic vascular resistance (SVR), pulmonary vascular resistance (PVR), cardiac output (CO), mean pressure of airway (Paw), dynamic lung compliance (Cydn), and arterial blood gases were measured during the observation period.

RESULTSNo piglet died in either group with severe lung injury. After four hours of ventilation, pH in the MV group gradually decreased to lower than 7.20, while in the PLV group, pH also gradually decreased but remained higher than 7.20 (P < 0.05). Partial pressure of oxygen in artery (PaO2) decreased in both groups, but with a significant difference between the PLV group and MV group (P < 0.05). Partial pressure of carbon dioxide in artery (PaCO2) increased in both groups, but with a significant difference between the PLV group and MV group (P < 0.05). Paw increased in both groups, but was not significantly different (P > 0.05). Cydn decreased in both groups, but without a significant difference (P > 0.05). At four hours, heart rate (HR) and MAP in both groups decreased. MPAP in both groups increased, and there was a significant difference between the two groups (P < 0.05). CVP was stable in both groups. At four hours, PVR and LAP were increased in both groups. CO was decreased in both groups (P < 0.05). SVR was stable during the observation time.

CONCLUSIONPLV did not improve outcome in changes of lung function.

Animals ; Liquid Ventilation ; Lung Injury ; chemically induced ; therapy ; Oleic Acid ; Swine

OBJECTIVETo observe the lung injury in rats induced by SiO₂ nanoparticles.

METHODSOne hundred and fifty SD rats were divided into five groups: the control group, the nanosized SiO₂ groups of 6.25, 12.5, 25 mg/ml, and the microsized SiO₂ group of 25 mg/ml, 30 rats each group. On the 7th, 15th, 30th, 60th and 90th day after exposure, six rats were sacrificed at each time point and the lung viscera coefficient, the pathological morphology and ultrastructure of lung were observed.

RESULTSAt each time point, the rat lung viscera coefficient of 25 mg/ml microsized SiO₂ and nanosized SiO₂ group were higher than the physiological saline group (P < 0.05), 25 mg/ml microsized SiO₂ group was higher than the same dose of nanosized SiO₂ group (P < 0.05); With longer duration of dye dust, lung viscera coefficient of 25 mg/ml microsized SiO₂ group and each dose of nanosized SiO₂ group were in time-effect relationship. Under light microscope we can see microsized SiO₂ group gradually formed cellularity nodules, and fused into fibrous nodules; At the early stage 25 mg/ml nanosized SiO₂ group occured focal alveolar macrophages and fibroblast proliferation and later fibrous connective tissue proliferated. Under TEM osmium lamellar corpuscle of type II alveolar epithelial cells were abnormal, and collagen and elastic fiber proliferated in mesenchyme of microsized and nanosized SiO₂ group.

CONCLUSIONNanosized SiO₂ particles after exposure can cause lung tissue injury in rat, and at the early stage it is showed inflammation, and later mainly characterized by pulmonary interstitial fibrosis differing from nodular lung fibrosis caused by microsized SiO₂, its ability to fibrosis is weaker compared with the same concentration of microsized SiO₂.

Animals ; Lung ; drug effects ; pathology ; ultrastructure ; Lung Injury ; chemically induced ; Male ; Nanoparticles ; toxicity ; Pulmonary Fibrosis ; chemically induced ; pathology ; Rats ; Rats, Sprague-Dawley ; Silicon Dioxide ; toxicity

OBJECTIVETo establish a canine model of severe smoke inhalation injury on unilateral lung, in order to observe the pathomorphological changes in the injured lung within 24 postburn hours (PBHs).

METHODSTwenty five mongrel dogs were employed in the study and randomized into 3 groups. The left lung was injured by inhaling smoke produced by burning sawdust with sparing the right lung with a breathing tube in 10 dogs in group A. A conventional model of smoke inhalation injury to bilateral lungs was reproduced in 8 dogs in group B, and dogs in group C not subjected to smoke inhalation served as controls. Hemodynamic changes, blood gas analysis and the pathophysiologic changes in the lungs were observed within 24 PBHs.

RESULTSAll of the dogs in groups A and C survived. Hemodynamic indices in the dogs in groups A and C remained stable without showing signs of systemic hypoxia. The arterial oxygen partial pressure in dogs of group A was 65 +/- 5 mm Hg, and the oxygen saturation in the mixed blood was 0.64 +/- 0.04 at 24 PBHs, and they were much lower than those in group C but higher than those in group B. The pathological changes in the injured side of the lungs in group A were similar to those in group B with high consistency, and the changes, though milder, could also be identified in the contralateral uninjured lung. Five dogs died in the group B within 24 hours after smoke inhalation and the survivors showed signs of multiple organ failure.

CONCLUSIONThe canine model of acute severe unilateral pulmonary smoke inhalation injury was reproduced reliably, and could be an ideal model for the study on smoke inhalation injury.

Animals ; Burns, Inhalation ; Disease Models, Animal ; Dogs ; Lung Injury ; chemically induced ; Male ; Random Allocation ; Smoke Inhalation Injury