The animal models of the combined injuries of mild, medium or severe hemorrhage and cyanide intoxication were produced by bleeding to 9.33, 6.67, or 5.33 kPa of arterial systolic pressure and administrating NaCN 2.5 mg/kg intravenously. Dogs with the combined injury of acute mild hemorrhage and cyanide intoxication in control group did not receive DMAP treatment whereas dogs in DMAP treatment groups receiveed DMAP 2 mg/kg iv at 3 min after administrating cyanide. The changes of hemodynamics and blood gases and methemoglobin were determined. The dogs receiving no DMAP treatnent in control group died within 5 min after intoxication. DMAP has an excitatory effect on hemodynamics after giving to dogs with the combined injury of acute mild hemorrhage and cyanide intoxication. It can save the dogs from death. The excitatory effect of DMAP on hemodynamics becomes weaker while the level of acute hemorrhage increases. The results of blood gas and methemoglobin analysis indicated that DMAP can disturb the oxygen-carrying capacity of hemoglobin because of the formation of much higher concentration of methemoglobin when DMAP is used as an antidote for the combined injury of acute hemorrhage and cyanide intoxication. The results suggested that methemoglobin formers should not be used as the antidotes for the combined injury of acute hemorrhage and cyanide intoxication.

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.

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.

With the development of economy and coming of information eva,the whole living space has been filled with electromagnetic wave with various frequencies.The chance of exposure to electromagnetic field for people grows with each pass-ing day.Environmental pollution by electromagnetic radiation has become the forth public muisance after the occurance of at-mospheric pollution,water pollution and noise pollution,and has brough t about the potential hazardous effects on the health of residents and individuals occupationally exposed to electromagnetic field.The effects of electromagnetic radiation on peoples health and living are versatile.The present paper mainly summarized the effects of electromagnetic radiation on neurobehaviour,electrocardiogram and oncephalogram in order to more understand the hazard of electromagnetic radiation.

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.

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.

In order to study the effects of soman intoxication on hemodynamics,the left ventricular pressure(LVP),the maximal changing rate of LVP(?dp/dt max),the aortic pressure(AP),the pulmonary arterial pressure(PAP),the cardiac output(CO),the cardiac index(CD and the heart rate(HR)were determined in anesthetized,chest -opened and mechanically-ventilated dogs at a simulated high altitude of 4 000m before and after an intravenous injection of 10?g/kg of soman.It was found that the toxicity of soman on cardiac functions was more severe at high altitude than at sea level.

Objective:To observe the clinical efficacy and adverse reactions of paroxetine combined with olanzapine in the treat-ment of depression complicated with sleep disorders. Methods: Totally 150 cases of sleep disorder patients were selected, and then randomly divided into the control group and the observation group with 75 ones in each. The control group was given paroxetine treat-ment, the observation group was given paroxetine combined with olanzapine treatment, and the treatment course was four weeks. The sleep latency, total sleep time, wake-up time and the number of awakening in the two groups were recorded, and the HAMD scale score and treatment efficacy were compared. Results:Compared with those in the control group, the sleep latency, total sleep time, wake-up time and the number of awakening in the observation group were obviously improved (P<0. 05). The clinical cure rate, the HAMD scale score and the incidence of adverse reactions between the two groups all had significant differences (P<0. 05). Conclu-sion:Paroxetine combined with olanzapine in the treatment of depression with sleep disorders shows fast efficacy, which can improve the sleep disorder symptoms and reduce the incidence of adverse reactions significantly.

Objective:To study the diagnosis values in severe acute pancreatitis (SAP) by means of the detection of C-reactive protein (CRP) and coagulation function in the early period of acute pancreatitis (AP). Methods:Seventy-two patients with AP accepted early detection of C-reactive protein (CRP),prothrombin time (PT),international normalized ratio(INR),activated partial thromboplastin time (APTT),fibrinogen (FIB ),CT scan and enhanced CT,and the evaluation on the CT severity index (CTSI). Results:There were significant differences in the levels of CRP,PT,INR,APTT,FIB and the CTSI scores between severe AP (SAP) and mild AP (MAP) (P

Objectives In this retrospective study we investigated the causes of misdiagnosis and incorrect treatment of hepatic cholangiocarcinoma and ways helpful in the improvement of correct diagnosis.Methods There were altogether pathollgy proved 40 cases of hepatic cholangiocarcinoma. The preoperative diagnostic procedures and surgical measurcs adopted were reviewed. Results The primary misdiagnosis rate was 68%. Patients were misdiagnosed as cholelithiasis complicated by intrahepatic inflammatory mass, hepatic abscess, hepatic hydrocyst, and hepatic adenoma;The surgical procedure performed were: choledocholithotomy, hepatophyma incision drainage or liver puncture drainage on B mode ultrasound localization, and hepatic cyst fenestration. Conclusions The hepatic cholangiocarcinoma can mimic many other benign diseases leading to misdiagnosis and improper surgery. Hence clinical features,history and laboratory evidence characteristic of the cancer must be sought preoperatively and intraoperative biopsy should be taken before definite surgical procedure. [