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Early severely burned rats and plasma endothelin Anisodamine (654-2 ) of _963

Started by wlsqfjaru, March 19, 2011, 03:57:56 AM

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Early severely burned rats and plasma endothelin Anisodamine (654-2) of
 
 
D) Statistical analysis: All data are Systat software applications,You are not allowed to view links. Register or Login, using a computer to analyze the data,You are not allowed to view links. Register or Login, said numerical order x ± SEM,You are not allowed to view links. Register or Login, P <0.05 significant level for the difference, P <0 A pair of very significant for the difference in standards. Second, the results (a) changes in burn plasma ET: B group after burn plasma ET content in the 2h peak, then decreased gradually; BA group plasma levels of ET after injury compared with B group (see Table 1) (b) of the burn changes in plasma LDH: serum LDH activity in the B group at each time point was significantly higher than those in NC group (P <0.01), and gradually decline. BA group at different time points after injury were significantly lower than B group (P <0 A pair), Table 2. China MEBO 4 / 20 007 Table 1 groups scalded rats before injury changes in plasma ET c8) after injury 【n = 8) C5966808B2394.8 ± 645 # # 2138.6 ± 1282 # 20471 = 9fi2 # # 14t47 ± 793 # # BAI625.3 ± I # # △ △ 1461.2 ± 926 # AA14081 ± 96.0j # △ △ 864.9 ± 49.1 △ △ and N 【group # # P <0. O1, compared with B maggots AZff '<0 A pair of the discussions (a) plasma burn El quickly increased and peaked 4 hours l4 our results observed increased within 6 hours after injury is obvious, and to 2h, which amounts to the peak. Rapid increase in plasma ET burn may be due to many factors, such as severe burns strong stress response, low blood volume caused by ischemia and hypoxia, cytokine, such as the role of tumor necrosis factor, oxygen free radicals can stimulate the body to produce a large number of ETLDH cell damage is reflected in the indicators. In this study, LDH was observed in all post-burn time points were significantly higher, indicating severe damage to tissue cells. Correlation analysis showed that El JI and other high-built 』_『 animal experiments confirmed that endogenous ET in the kidney after burn injury. We believe that ET is an early stage of burn-induced injury of the more important factor (the role of two possible new mechanism for 1654-2 :654-2 antibody grams of mechanisms that can protect cells at the cellular level to improve the cells to ischemia and hypoxia tolerance, stability, subcellular structure and reduce the shock factor of production, the cells mainly through the mechanism of calcium antagonism, the results show that :654-2 can inhibit the effect of elevated ET. at the same time increase in the inhibition of ET also reduced the extent of cell damage. 6542 inhibited the increase of plasma ET, may directly inhibit the expression of ET release, or to mitigate damage cells indirectly reduce the production of ET, or both, remains to be elucidated. guess 6542 to protect cells in the antibodies grams of mechanisms of action may be related with the inhibition of Eq.

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