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 effects of 4-DMAP and NaNO2 on the hemodynamics of dogs suffering from acute hemorrhage complicated with cyanide poisoning were studied. It was found that the administration of 4-DMAP could brought about an increase of the cardiovascular functions in the experimental animals. Although the increase was temporal and not very impressive, it played an important role to prevent the dogs from developing cardiovascular collapse during the period of observation. On the other hand, the administration of NaNO2 resulted in a transient excitation for 1-2 minutes and then a prolonged and progressive depression of the cardiovascular functions, and all the experimental animals died from cardiovascular failure within 13-19 minutes after NaNO2 injection.The results of this study indicate that 4-DMAP as a therapeutic agent for acute hemorrhage complicated with cyanide poisoning is superior to NaNO2 since the former can produce an excitation of the cardiovascular functions while the latter a progressive depression and eventually a failure of the cardiovascular functions.