ABSTRACT
The preventive effects of some drugs on pulmonary lipid peroxi-dation and inborn oxidation protectant system in the lungs were observed in rats after the animals were exposed to 200 ppm of hydrogen sulfide (H2S) for 3 hours.Malondialdehyde (MDA) level of the lungs and bronchoalveolar lavage fluid (BALF),superoxide dismutase (SOD) activity,glutathione(GSH) and vitamin E (VE) levels of the lungs were determined in the 6th and 12th hour after H2S inhalation.It was found that a significant increase of MDA level of both the lungs and BALF and a significant decrease of SOD activity and GSH and VE level occured after a single exposure to 200 ppm of H2S inhalation.On the contrany,the MAD level of every group of which the animals had been medicated for prevention was lower than that of the intoxicated groups.Among the premedicated groups,the MDA level of 4-dimethylaminophenol(DMAP) group,VE group,and NaNO2 group was not different from that of the normal except that the MDA level in BALF was higher in VE and NaNO2 group than in the control.In every premedicated groups,SOD activity was increased and GSH and VE levels were elevated.These facts suggest that DMAP,NaNO2,VE,dexamethasone and anisoda-mine all could reduce the MDA level and elevate the capacity of the oxidation protectant system of the lungs after H2S inhalation.It is concluded that there are drugs to protect victims from H2O intoxication while DMAP,NaNO2 and VE are relatively more potent among the drugs used in this study.
ABSTRACT
The role of free radicals in the precipitation of lung damage after hydrogen sulfide inhalation was investigated in rats, which were killed right after and in the 1st, 6th,12th, 24th, and 72nd hour after exposure to 100 and 220 ppm of hydrogen sulfide (H2S) for 3 hours respectively. Malondialdehyde(MDA) level in lung homogenate and in bronchoalveolar lavage fluid (BALF), protein content and the number of leucocytes and pulmonary alveolar macrophages (PAM) in BALF, superoxide dismutase(SOD),glutathione(GSH),and vitamin E(VE)level in lung tissue and blood were determined. It was found that H2S inhalation resulted in an increase of MDA level which occurred much earlier after exposure to 220 ppm than after exposure to 100 ppm. Protein content was increased in the 1st, 6th, and 12th hour after inhalation. The number of leucocytes and PAM were increased, which implies the existence of inflammatory response in the respiratory tract. SOD activity decreased in the early period after inhalation but significantly increased later. Both GSH and VE levels decreasedThese findings suggest that H2S inhalation induces an inflammatory response in the respiratory tract and an increase of free radical formation which in turn brings about exessive lipid peroxidation. It is concluded that free radical formation is a contributing factor of lung damages after H2S inhalation.
ABSTRACT
The pulmonary toxicology after H2S inhalation was studied with bronchoaleveolar lavage (BAL),ultracentrifuge.and optical and electron microscopy in rats.The changes of the activities of lactate dehydrogenase,alkaline phosphatase,acid phosphatase and angiotension converting enzyme in BAL fluid were used as indicators of cellular damages.those of leucocytic count as the indicator of inflammatory response,and those of the concentration of protein and Evans blue as the indicator of the alterations of vascular permeability.In addition,the effects of H2S on lipid peroxidation,natural antioxidative system and energy substances and the changes of phospholipid concentration in BAL fluid were also studied.The results were as follows:(1)Inhalation of H2S exerted a severe cytotoxic effect on the lung tissues resulting in damages on various types of cells and a severe edematogenic effect on lung parenchyma.(2)The development of pulmonary edema in H2S intoxication resulted from a combination of different pathogenic factors.(3)The biochemical changes and their recovery occurred earlier than those of the pathological changes.The effecacy of 6 categories of drugs including 25 medicaments against H2S intoxication was e-valuated in mice,and 10 drugs were found prophylactically effective.The effects of various methe-moglobin-forming substances and some other drugs were also investingated in their treatment for H2S intoxication in rabbitsand dogs.It was concluded that methemoglobin-forming substances could be used as specific antidotes but could not prevent or diminish the lung damages due to H2S inhalation unless they were administered in association with dexamethasone,vitamin E,and anisodamine.Eventually,a postulated scheme of the medical treatment for H2S intoxication was presented.
ABSTRACT
The pathological changes of the lungs after a single exposure to an atmosphere containing 100?15 ppm of hydrogen sulfide(H2S)for 3 hours were observed with optical and electron microscopy in rats.It was found that bronchial epitheliem,alveolar epithelium,pulmonary vessels and pulmonary interstitium were extensively involved.Pulmonary edema,focal pulmonary hemorrhage,exfoliation of the damaged epithelium,and infiltration of neutrophils occurred mainly in the 3rd hour to the 3rd day after H2S intoxication.Chronic inflammatory response and proliferation of fibrous tissue occurred mainly from the 7th to the 15th day after intoxication.Ultrastruc-turally,there were marked changes of alveolar epithelium,phagocytes,vascular endothelium,fi-broblasts,and inflammatory cells.Initial pulmonary edema emerged in the pulmonary interstitium and gradually affected the alveoli.Fragments of alveolar surfactant could be seen in the 3rd hour to the 3rd day after intoxication.These findings indicate that H2S inhalation exerts extensive injurious effects on the lungs in the rats.