The toxicity of HCN was determined first.The experimental animals were intoxicated with a HCN concentration of 1103.8?48.32 Y/L and were exposed for 4.55?2.04 minutes.The mortality rate in 24 hrs was recorded.The LDEO,sLD50,and LD99 were calculated as 844.31?/kg,172.39?/kg and 959.18?/kg respectively.Two preparations of DMAP injection were found to have preserved rather good anti-HCN potency even though they had been kept under room temperature for about one year.All the 11 dogs survigd a dose of 4 LD50 of HCN in halation poisoning when DMAP was injected intramuscularly 1 minute after exposure.Another 5 dogs inflicted with similar HCN intoxication were also all saved when intravenous DMAP injection was given at the time of respiratory arrest. The cyanide level in the blood of the dogs after inhalation of HCN was determined by spectrophotofluorometry with pyridoxal.The blood concentration after inhalation of a lethal dose of HCN was 110?26.6?/100 ml at the moment of respiratory arrest.DMAP after intramuscular injection can shift the cyanide combined with cytochrome oxidase to red blood cells to form ferrihemoglobin cyanide,and cell respiration is then restoredEventually the dogs could survive the 4 LD50 HCN intoxication.

Stroma-free methemoglobin solutions were prepared from dog and pig red blood cells. The procedure is based on oxidizing the ferrous iron in hemoglobin solution to the ferric state. Then all the cell membrane components (i.e.stroma) were removed through crystallization of the hemoglobin molecule in high ionic phosphate buffer, dialysis and repeated washing of crystals prior to solubilization. This method is feasible and reproducible. The methemoglobin solution obtained had similar potassium, sodium, chloride ion concentration and pH value as normol serum. Spectral maxima and minima were characteristic for methemoglobin.SFMS proved to be an effective antidote for cyanide intoxication. Its protection ratio was calculated to be 2.25 while the rats were treated with SFMS equal to 7 % of their total body hemoglobin. The potential advantages of SFMS over current antidotes include its immediate action with cyanide and doesn't compromise any of the patient's oxygen carrying capacity. In preliminary work, SFMS was given at levels of 4-10% total hemoglobin with little adverse effects.

The effects of acute hemorrhage complicated with cyanide posisoning on the hemodynamics were studied and compared with those simple cyanide poisoning in 24 dogs.Cyanide poisoning was induced by intravenous injection a lethal dose of NaCN of 2.5mg/kg,Acute hemorrhage was created by bleeding the dogs to an arterial pressure of 9.33 kPa(70mm Hg)within 2 minutes through a cannulated femoral artery.HR,CO,MAP,LVP,LVP (?)dp/bt max,and ECG were recorded.It was found that the excitatory response of cardiovascular functions was observed within 1 minute after cyanide poisoning,then a significant failure of the cardiavascular functions resulted in the rapid death of the animal 7~10 minutes after cyanide administration.In case when cyanide poisoning was complicated with acute hemorrhage,no excitatory response of the cardiovascular functions could be observed.An early cardiovascular collapse occurred which was characterized by a rapid fall of CO,MAP,LVP,LVP(?)dp/dt max as well as arrhythmia.All the dogs in this group died of acute failure of cardiovascular functions 4- 6 minutes after cyanide poisoning.The results of this study suggest that the failure of the cardiovascular functions is the main cause of death in case of acute hemorrhage complicated with cyanide poisoning.

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.

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.

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.

The toxicity of HCN inhaled via the respiratory tract in dogs and the therapeutic effects of DMAP and AmNO2 for such form of HCN intoxication were studied. The LD50 of HCN when inhaled was 850.4?80.4?g/kg.When the dosage of 2?LD50 of HCN was given to the experimental animals, the signs of intoxication developed rapidly. Uneasiness, struggling, strident barking, and respiratory excitation were observed several seconds after the exposure. Subsequently there was spasm of the extensors and rigidity of the extremities. Finally general inhibition and paralysis ensued. Respiration and heart beat stopped 6 and 7 minutes after exposure. If DMAP (3.25 mg/kg intramuscularly) or AmNO2 (2 ampules through inhalation) was administered 15 seconds after exposure, the survival rate of the animals was 90% or 100% respectively.When the dosage of 4?LD50 of HCN was inhaled and the two drugs were administered 45 seconds after exposure, the survival rate of the animals treated with DMAP remained as high as 90% (9/10) .But the survival rate of those treated with two ampules of AmNO2 or even three ampules reduced to 20% or 40% respectively.The amount of HCN inhaled during respiratory intoxication, the problems of early diagnosis and the administration of DMAP at the site of accident were analyzed and discussed.