A Research In Secondary Renal Injury Of Traumatic Hemorrhagic Shock Swine Model In Dry-heat Atmosphere

Background: This paper through establishment the model of pigs of dry-heat environment of traumatic hemorrhagic shock of desert to study that the pathophysiology feature and changes of renal injury under the dry-heat environment with traumatic hemorrhagic shock.At the same time,the effect of apoptosis and inflammation on the kidney injury of dry-heat environment with traumatic hemorrhagic shock was discussed,and to provide a theoretical basis for clinical treatment.Methods: A total of 68 healthy male Landrace piglets were divided into 3 groups by random number table: the traumatic hemorrhagic shock of dry-heat environment shock(DHS,n=24),the sham operation group of dry-heat environment control(DHC,n=20)and the traumatic hemorrhagic shock of normal temperature environment shock(NTS,n=24).The DHS group and DHC group were exposed in experimental cabin for 3 hours(40.5°C±0.5°C,10%±2% humidity),and each groups were average divided into 4 subgroups: T0(after expose 3 hours in cabin),T1(50min after the success of the model),T2(100min after the success of the model)and T3(150min after the success of the model).NTS group was also exposed in the cabin for 3 hours(25°C±1°C,50%±5% humidity),The NTS group was divided into 4 subgroups,and the specific time points were consistent with those of DHS group and DHC group.Establishment of traumatic hemorrhagic shock model in dry-heat environment,collected blood to test BUN,Creatinine;collected urine to inspect NGAL;collected kidney tissue to evaluate the renal tissue morphology and detect the expression of protein JNK,Caspase-3 and Cytochrome c.Results:(1)Compared with NTS group,DHS group in dry-heat environment after 3 hours of exposure,BUN and Scr levels increased,but there is no significant difference(P>0.05).With the prolongation of time,renal damage index increased more and more obvious.Compared with DHC group,the DHS group showed significant difference in T2 time(P<0.05);(2)Compared with NTS group,DHS group in dry-heat environment after 3 hours of exposure,urinary NGAL increased slightly,but the difference was not statistically significant(P>0.05),50 min model is statistically significant(P<0.05).Compared with the DHC group,the DHS group at the beginning of T1 were statistically significant(P<0.05).(3)As the exposure time prolonged by dry-heat environment,the kidney gradual emergence of Bowman cavity expansion,cavity shedding degeneration necrosis cells,renal tubular epithelial cell edema under the light microscope.Combined dry-heat environment with traumatic hemorrhagic shock showed glomerular capillary hyperemia,expansion,edema,degeneration of renal tubular epithelial cells,exfoliated epithelial cells with Bowman cavity the distal tubule epithelial cell shedding.(4)Compared with NTS group,the DHS group expression of IL-1,IL-6,IL-10 and TNF-? in dry-heat environment after 3 hours of exposure began to increase and there is significant difference(P<0.05),compared with the DHC group,DHS group showed the differences(P<0.05)at T1 time point.(5)Compared with NTS group,DHS group exposed to dry-heat environment after 3 hours,the expression of JNK-2 began to increase and has a statistically significant difference(P<0.01),but no significant difference between the expression of Cytochrome C and Caspase-3(P>0.05),and there were significant differences(P<0.01)at T3 time point.Compared with DHC group,DHS group in dry-heat environment exposed 3 hours no difference,but at T3 time point,the index expression of DHS group were significantly increased and had statistical differences(P<0.01).(6)Compared with NTS group,DHS group in dry-heat environment after exposure,there was no significant difference in cell apoptosis(P>0.05).At the T1 time point,the rate of apoptosis was significantly increased,and the difference was statistically significant(P<0.01).Compared with DHC group,the apoptosis rate at T1 time point was significantly increased,and has statistical difference(P<0.01).Conclusion: When the dry-heat environment combined with traumatic hemorrhagic shock,dry-heat environment and traumatic hemorrhagic shock driven the expression of inflammatory and apoptosis induced by mitochondria play an important role in renal injury.It can accelerate the damage of renal glomerulus and renal tubule,and make the renal function worse,and lead to the occurrence of acute kidney injury.