| "Cardiac shock", occurring at the early stage of severe burns, is not only the pathophysical basis of inducement and aggravation of burn shock, but also the main cause of ischemia/hypoxia and dysfunctions of other organs. Previous studies indicated that ischemia and hypoxia was the confluent point of tissue and cell damages at the early stage of severe burns. The mitochondria is not only an important organelle to provide the energy-ATP for cells through oxidative phosphorylation, but also takes part in the protein syntheses through mtDNA by self-transcription, replication, and expression. mtDNA involves in the encoding 13 peptides of 4(COX,F0,F1-ATPase,NADH and cyt b) among the 5 key enzyme complexes in oxidative phosphorylation. In this way, mtDNA plays an important role in the oxidative phosphorylation.In the present study, the mtDNA damage of burned rats at the early stage was investigated to identify the role of mitochondria in the occurrence of "Cardiac shock"; And to clarify whether the damage of mtDNA was alleviated and the mechanisms of the amelioration of "Cardiac shock" after taking en masse escharectomy at the early stage of severe burns,Meterial and Methods:66 Rats inflicted with 30% TBSA of full-thickness burns were used in this study, Rats were randomly divided into normal control group,non-escharectomy group and escharectomy group. All animals were infused with balanced salt solution according to Parkland's formula. Rats in escharectomy group underwent escharectomy en masse and the wound was coverd with fresh alloskin immediately 20 minutes following burns. The changes of SOD activity and MDA content in myocardial tissue were examined at pre-burn and 1,3,6,12,24 hr post-burn; Myocardial mtDNA was detected for 4.8kb deletion with semi-quantification PCR; The content of ATP,ADP and AMP in myocardial mitochondria and Tn I in serum were also determined. Results and conclusion:1. In the burn rats, level of SOD activity decreasd obviously, reached the minimum at 6 h, recovered slightly at 12 h and decreased again at 24 h. While MDA content was increased rapidly at 1 h after burn, reached the lowest at 6 h, returned to normal at 12 h but increased again at 24 h. 2. At 1 and 3 h after burns, 4.8-kb deletion of mtDNA in the deletion type region were found in some rats, showing heterogeneity, There was no deletion of mtDNA in 6 and 12 h post-burn; At 24 h after burns, however, there were full deletion in myocardial mtDNA. This characteristics was consistent with the peroxidative damage and suggested that the mtDNA deletion is induced by it.3. The ATP content in myocardial mithochondia began to fall down obviously at 1 h after burns, reached the minimum at 6 h, recovered slightly at 12 h and decreased again at 24 h. Level of ADP was significantly increased at 3 h, reached its peak at 12 h and remained at a high level at 24 h. changes of AMP level were similar to those of ADP, suggesting that the deletion of mtDNA affected the oxidative phosphorylation and lead to the decreased production of ATP. This may be main reason for the disturbance of energy metabolism in myocardial tissue of burned rats.4. the content of Tn I in serum was elevated dramatically at 1 h after burns and came to the summit at 6 h, slightly recovered at 12 and 24 h , which was consistent with pathologic changes of myocardial tissue. All of which suggested that the decreased ATP production is the important cause of myocardial damage at the early stage of severe burns. 5. After escharectomy en masse at the early stage of severe burns, a mild decrease of SOD activity and increase of MDA content were found only within 3 h post-burn, and then recovered gradually. There was a significant difference between escharectomy group and non-escharectomy group, suggesting that escharectomy en masse alleviated the peroxidative damage to myocardium after severe burns in rats.6. After escharectomy en masse at the early stage of severe burns, the deletion rate of myocardial mtDNA was decreased. Compared with the non-esch...
|
PDF Full Text Request