To Explore The Causes Of Death Of Acute Paraquat Poisoning In Mice

Objective: To investigate the paraquat (paraquat, PQ) poisoning in miceacute period (5days) the cause of death.Methods:120Kunming mice (SPF fed)(half male and half female,20-23g),were randomly divided into2groups: normal control group (N group, n=20rats), poisoning group (PQ exposure group, n=100Only). Poisoning group:110mg/kg (median lethal dose [1]) PQ disposable gavage,physiological saline ingroup N were orally given a corresponding amount of weight. Start the generalobservation of the two groups of mice for5days, group N (daily executed2-4only) comparison of anatomical and pathological slices and stained with HE foreach dayof different organs and various organs, and64died in group PQmicebody, change the body signs and pathological observation.Results: the normal group: activity, spirit, diet, body each organ pathologyimaging of normal, normal. Poisoning group:(1)6464%deaths, the mortalityrate.(2) eye view: gradually appear static voltmove less, look dull, sluggish,arch back, shortness of breath,cyanosis and other performance; the body showedsigns ofsystemic skin loose and shed, scattered in the tail skin bruising,punctatehemorrhage, heart, lung, liver, kidney, spleen, small intestine, color, dark red,the most obvious changes in the lung.(3)compared the different organs under light microscope: the first day:to lung and moderate inflammation is heavy,pulmonary hemorrhage, pulmonary interstitial thickening, then part of renaltubular cells edema and a small amount of protein tube, heart edgeedema, theother organs are mild; second days: most pulmonarymild inflammation, amoderate inflammation, emphysema,pulmonary clearance thickening, fiberhyperplasia, heart from mildedema dissolved to about60%and a small amountof about10%~60%of liver necrosis, edema, a handful of renal tubular celledema and protein cast, spleen intestinal disease slightly, with heart and lunglesions in both the main; third days: pulmonary inflammationand moderateinflammation proportion close dissolution of heart cells, about more than30%,liver and kidney lesions, spleen bruise in20~50%more congestion, smallintestine villi in the small shed,heart disease with pulmonary lesions weightbased. The fourth day:most pulmonary inflammation, the most heart dissolved50%, liveredema serious, most kidney small protein tube, a handful of renaltubular edema;60%splenic congestion, more than half of the remaining range,slight congestion, intestinal cells edema, withheart disease with pulmonarylesions weight based. The fifth day:2/3lung moderate inflammation,1/3mildinflammation, mild cardiacedema, congestion and edema of liver and spleenliver kidney than before to reduce, no protein tube edematous and cell, smallintestinal disease slightly.(4) in different organs of differentfluorescentmicroscopic pathological changes were: lung: a mild to moderate inflammatory,pulmonary hemorrhage and pulmonaryseptal thickening, changes of emphysema,fibrosis, edgecongestion,: the first day, second days to lose, third days, fourthdays and fifth days to reduce, increase. Heart: the first day of the left edge of thecell lysis, the second day dissolution range, reducethe weight of third days,fourth days later, slightly heavier than thesecond days, fifth days a slight edge of myocardial edema,congestion. Liver: the first day a little hydropic degenerationandfatty degeneration, slight congestion edema; second to expand the scope ofarticle three or four days, most heavy, about80%of liver edema (60%above),the fifth day and edema was significantly relieved. Kidney: the first day oftubules mild edema, renal smallminority protein tube, third days is the heaviest,most kidney smallprotein tube, fifth days no protein tube oedema and cell.Spleen: the first day after one side edge congestion, aggravate, articlefourth daysabout60%splenic congestion, more than half of1/3range, fifth days wereobvious congestion, intestinal: in addition tothird days a small intestinal villusshedding, fracture, fourth days ofintestinal cells edema, the rest of the day werenot obvious.Conclusion: in the acute stage of mouse heart, liver, lung, kidney,intestine,spleen in varying degrees of damage of paraquat poisoning, which is dominatedby heart and lung lesions: bothmyocardial cells showed different degrees ofdissolved, lung showed mild to moderate inflammation, hemorrhage andalveolar wall thickening of pulmonary emphysema, a small amount of fiber inother organs and different; the degree of congestion, liver and kidney cells ofrenal tubule hydropic degeneration, a small amount of protein tube, intestinalcells edema, lesions are relatively lighter.Acute mortality of mice64%the paraquat poisoning, death may bemostmajor due to myocardial cell lysis due to heart failure, andrespiratory failurecaused by acute lung injury induced by acute lung injury, few because ofrespiratory failure caused by. Study onacute paraquat poisoning to provide theorgan level on the basis ofunderstanding of death, to improve the paraquatpoisoning in patients with acute cerebral pathological changes and deathhelp,thus early diagnosis and treatment.