Whole thickness burn (20% TBSA) was produced in adult rats of Wistar strain.The animals were divided into two groups: In the first group,liver mi-tochondrial respirarorv function was determined polarographically on the 9th day postburn (PB).In the second group,burn eschar was removed 9 days PB and extracted with physiological saline.Extract of normal rat skin was prepared in a similar way- Liver mitochondria were prepared from normal rats and incubated with serial dilutions of the extracts of eschar and normal skin respectively.The respiratory function was then determined.It was found that the respiratory control ratio (RCR) in the burn group was much depressed (63.7% as compared to normal).State 3 respiration rate also decreased (71.09% viz normal) but state 4 slightly increased.The differences were very significant (P

20% TBSA full thickness burns was inflicted on the back of rats with a 5 KW bromotungsten lamp. The animals were sacrificed on the 1st, 2nd, 3rd, 5th, 7th, and 9th day post-burn. Then the lipid peroxide and Vitamin E contents of the plasma, eschar and liver homogenate, mitochondria and microsomes were determined. It was found that the lipid peroxide content of the plasma and eschar increased postburn. The elevation of lipid peroxide level in the escbar showed 2 peaks on the 2nd and 7-9th day postburn and was related to the positive bacterial culture of the sube-schar tissues. The changes of the lipid peroxide levels in the mitochondria and microsomes were similar to those in the eschar. The elevation of plasma lipid peroxide showed only one peak on the 3rd day postburn. The vitamin E levels in these tissues decreased markedly after injury, reached the lowest point 3-5 days after burns, and maintained at a low level throughout the whole course of observation.The causes of the increase of lipid peroxidation and its damage to the subcel-lular structures were briefly discussed.

Lipid extract of burn eschar (D_1) added to isolated rat liver mitochondrialcaused depression of respiratory control ratio (RCR), ADP/O ratio, rate of ATP produc-tion, respiration rate in state 3 but it stimulated the respiration rate in state 4. Pretreat-ment with vitamin E significantly prevented the inhibition of mitochondrial respiratoryfunction caused by D_1. The addition of vitamin E after that of D_1 had no protective ef-fect. Heat-treatment of D_1 markedly reduced its inhibitory effect on mitochondrial respira-tory function. Cumene hydroperoxide (CHP) markedly depressed mitochondrial respiration.Vitamin E caused a significant increase in RCR, which was inhibited by CHP at lowerconcentrations. Vitamin E reduced MDA formation considerably in normal mitochondriaand in those mitochondria incubated with D_1, heated D_1 or CHP. These findings indicatedthat D_1 -and CHP-induced depression of mitochondrial respiratory function was probablydue to lipid peroxidation damage which was proved by the protective effct of the pota-tive antioxidant vitamin E.

Cumene Hydroperoxide(CHP)-induced mouse mitochondrial lipid peroxides (LPO) are significantly higher than those of the normal mitochondria ( P

Rats were divided into 3 groups and inflicted with total body irradiation of 5 Gy of gamma rays from a 60Co source,15% TBSA full thickness burns,or both of them respectively.The changes of lipid peroxide,cytochrome oxidase,NADH-cytochrome C reductase,catalase and superoxide dismutase activities were observed.It was found that the MDA content of hepatic mitochondria was significantly elevated in all the 3 goups on the 2nd and 6th day postinjury,and there was a third peak of MDA elevation in the the burn group on the 10th day postinjury.The increase of MDA in hepatic mitochondria was probably due the combined action of 2 factors.(1) increased production of toxic active oxygen species such as O2-and H2O2 as a result of increased activity of NADH-cytochrome C reductase and cytochrome oxidase,and (2) alterations of the defence mechanism against this active oxygen species due to lowered activity of superoxide dismutase and catalase.

Male mice were subjected to 6 Gy total body irradiation,20% TBSA full thickness burns,or both the injuries respectively,and then lipid peroxides (LPO),vitamin E,sulfhydryl groups,respiratory control ratio (RCR),ADP/O ratio,and cytochrome oxidase activity of hepatic mitochondria were determined in the animals in the first 9 postinjury days.It was found that.1.LPO level increased in the early postinjury stage in the combined radiation-burn injury group.2.Vitamin E level decreased significantly in both the groups with either only irradiation or burns.3.The sulfhydryl groups showed a tendency to increase in all the 3 groups.4.The activity of cytochrome oxidase increased signficantly on the 7th postinjury day in the combined injury group.5.RCR and ADP/O ratios decreased more significantly in the combined injury group than in either the single injury group.These facts suggest that the suppression of the respiratory function of hepatic mitochondria results from the damage of mitochondrial membranes due to iipid peroxidation.

The fatty acid content of liver mitochondria was quantitatively determinde with gas chromatography in rats after they were inflicted with 15% TBSA full thickness burns or after the liver mitochondria were incubated with lipids extracted from eschar tissue(D1)or from normal skin of rats(D'1).It was found that after burn injury,the content of unsaturated fatty acid of liver mitochondria decreased and that of saturated fatty acid increased significantly.Both Dl and D'l decreased the content of unsaturated fatty acid and the decrease would be more significant when the concentration of eschar lipids or skin lipids was increased.D1 reduced the unsaturated fatty acid content more significant than D'1 when the two were in same concentration.The possible mechanism of the decrease of unsaturated fatty acid in the liver mitochondria induced with burn injury,eschar lipids or normal skin lipids was discussed briefly.

OBJECTIVETo investigate therapeutics for and the pathological basis of combined radiation and burn injuries.

METHODSCombined radiation and burn injuries on mice and rats were inflicted by gamma ray irradiation from a (60)Co source and thermal radiation from a 5 kW bromotungsten lamp.

RESULTSThe dysfunction of myocardium played an important role in the development of early stage shock. Transfusion of irradiated (in vitro, 20 Gy) or stored (4 degrees C, 7 days) blood after irradiation was done to promote the success of allo-transplantation of bone marrow. Decrease of IL-4 mRNA expression was the molecular basis of depression of intestinal mucosa immune and intervention of IL-4 showed an antagonistic effect on enterogenic infection. A new lipid component extracted from burn eschar was documented for the first time and its toxic effects were elucidated. The survival rate of alloskin grafts after removal of burn eschar from the recipient animals was obviously increased in combined injury due to reduction of immune rejection activity by the radiation effect. In contrast, in animal models with simple burn, the alloskin grafts were all rejected within ten days after the procedure. A successful therapeutic result (survival rate: 92% for 30 days and 67% for 100 days) was obtained by comprehensive management of treated animals, while the untreated control animals all died within 3 - 7 days after injury.

CONCLUSIONThe pathogenesis of injury caused by simultaneous radiation and burn is extremely complicated and the treatment is very difficult. A comprehensive management program consisting of several therapeutic measures aimed at key links of the pathogenesis may achieve significantly improved results.

Animals ; Burns ; pathology ; physiopathology ; therapy ; Calcium ; metabolism ; Heart ; physiopathology ; Hematopoiesis ; Mice ; Radiation Injuries ; pathology ; physiopathology ; therapy ; Rats ; Rats, Wistar