Intervening Effects Of Oxygen-enrichment On NaCN Intoxication Of Hypoxia Dogs

Hydrogen cyanide（HCN），a widely used high toxic industrial chemical, has long beenemployed as a chemical warfare agent since the First World War（WWI）. Its intoxicationeffects are potent, quick and hard to defend. After the cyanogens agents enters the body, theCN ion stops cells from performing respiratory functions and oxidative phosphorylation. Itinhibits oxidizes the end of the mitochondrial respiratory chain. This causes the tissues todie due to lack of toxic lack of oxygen. Also known as damage to “internal respiratory”.Therefore, people with cyanide intoxication will die from respiratory failure and circulatoryfailure within minutes.There is a vast plateau region in our country and it is very important for our country.Hypo baric hypoxia at high altitude is the main feature of the environment. Hypoxia cancause abnormal reaction and also increase the damage of chemical poisons on the brain,heart and lung. People occurred cyan amide poisoning in the plateau will suffer more severedamage because the body will suffer from respiratory hypoxia and cell hypoxia. Nowpeople have little knowledge about cyanide poisoning under the condition of hypoxia.Based on the previous studies, this research is to study the injury effect on heart ofcyanide poisoning under the condition of hypoxia and the prevent effect of oxygen-enrichment on it. First we use dogs as the experimental subjects. Animal model of acutehypoxia is established through breath the nitrogen-oxygen mixture gas. The biologicaleffects of the model is evaluated; second, based on this hypoxia model, the model ofhypoxia and NaCN intoxication is established; third, the prevent effects of oxygen-enrichment on the model is evaluated.Methods:1. Dogs were used as the experimental subjects. Animal model of acute hypoxia isestablished through breath the nitrogen-oxygen mixture gas. The biological effects of the modelis evaluated through examined the parameters such as HR, LVSP, PaO₂,+dp/dtmax, and so on. 2. Using the model that established in experiment1, we established the the model ofhypoxia and NaCN intoxication. Control group and hypoxia group were setted. Receded theheart parameters in-60min,0min,10min,30min,60min,80min and120min.3. Using the models in experiment2, divided the dogs into two groups: oxygen groupand hypoxia group. Dogs in hypoxia group continuous breath the nitrogen-oxygen mixturegas while dogs in oxygen group breath the oxygen-enrichment gas. Receded the heartparameters in-60min,0min,10min,30min,60min,80min and120min.Results:1. Model establishment of dogs suffer from acute hypoxia1.1Effects of acute hypoxia on ECG parametersCompared to the control group, after breath the nitrogen-oxygen mixture gas, HR ofanimals in the hypoxia group showed a significant changes, PQd interval and QRS wavewas significantly shorter.（P<0.05）.1.2Effects of acute hypoxia on left ventricular pressureCompared to the control group, after breath the nitrogen-oxygen mixture gas, themagnitude of changes of LVSP,+dp/dtmax, LVEDP were increased. At the end of theexperiment these parameters were significant low than the control group（P<0.05）.1.3Effects of acute hypoxia on arterial bloodCompared to the control group, after breath the nitrogen-oxygen mixture gas, the pH ofhypoxia group was increased. The PaO₂andSaO₂were significant decreased （P<0.05）.2. Effects of hypoxia and cyanide poisoning on the function of heart.Experiments showed that both the normal and hypoxia state, cyanide poisoning cancause heart damage, mainly in the heart rate reduction, PQd and QRS interval fluctuations,left ventricular pressure and blood oxygen saturation decreased and Arterial oxygen tension（PaO₂）, arterial oxygen saturation （SatO₂） fluctuates significantly. Compared with controlgroup, the parameters of the hypoxia group, such as HR, left ventricular pressure and bloodoxygen saturation, Arterial oxygen tension （PaO₂）, arterial oxygen saturation （SatO₂）decreased more significantly. The effects of combined hypoxia and NaCN intoxication onthe heart function of dogs are even worse.3. Intervening effects of oxygen-enrichment on NaCN intoxication of hypoxia exposed dogs.Breathing oxygen-enriched air is effective for animals of acute hypoxia after cyanidepoisoning. It significantly inhibited the heart rate reduction and improved PQd and QRSwaveform. The mLVSP and+dp/dtmax, which reflect the heart function, were alsoimproved. Blood gas analysis also showed that, compared with the hypoxia group, theoxygen-rich group of arterial oxygen tension （PaO₂）, arterial oxygen saturation （SatO₂）decline slows, blood pH fluctuations smaller. This reflects the oxygen therapy can enhancemyocardial contractility, protect the heart function.Conclusion:1. Animal model of acute hypoxia is established successfully through breath thenitrogen-oxygen mixture gas.2. Both the normal and hypoxia state, cyanide poisoning can cause heart damage. Theeffects of combined hypoxia and NaCN intoxication on the heart function of dogs are evenworse.3. The oxygen therapy can enhance myocardial contractility and protect the heartfunction.