ABSTRACT
AIM: To investigate the variation of nitric oxide(NO) and NO synthase(NOS) in rats during the early stage of severe burn and their possible relation with prognosis of severe burns.METHODS: Levels of NO - 2/NO - 3, the metabolic products of NO, nNOS and iNOS protein in brain, lung and duodenum of rats were measured before and after burns. Survival times of rats in each group were also measured.RESULTS: Levels of NO - 2/NO - 3 in rats after burn increased remarkably, selective inducible NOS( iNOS) inhibitor aminoguanidine (AG), and nonselective NOS inhibitor L-NAME can inhibit this increasing. Levels of neuronal NOS(nNOS) protein in normal rats were low, and iNOS could not be detected. Levels of nNOS protein increased mildly in all observed tissues and the levels of iNOS protein increased remarkably after burn. Administration of L-NAME and AG made the increase of nNOS more apparently but could not affect the level of iNOS. Survival time of rats decreased in L-NAME group and increased in AG group compared to control group.CONCLUSION: Symptoms such as vascular ralaxation and hypotension in burn shock are connected mainly with over-increased iNOS. [
ABSTRACT
AIM: To study the effect of cGMP-dependent protein kinase (PKG) on the pathogenesis of burn shock. METHODS: Confluent endothelial cells were disintegrated and centrifugated to obtain cell lysates after being treated with 10% burn serum or PKG activator 8-Br-cGMP. PKG activity of lysates was measured with radioactive isotope label method in a reaction system of phosphorylation of specific substrate H2B by PKG, and the shape and the distribution of intracellular filamentous actin were detected by specific fluorescence staining. For the control study, the PKG specific inhibitor KT5823 were used to pretreat the endothelial cells before the administration of burn serum or PKG activator 8-Br-cGMP. RESULTS: Exposures to burn serum and 8-Br-cGMP led to a rapid time-dependent increase in endothelial PKG activity and the polar distribution of intracellular filamentous actin, and preincubation with KT5823 abolished those effects. CONCLUSIONS: The results suggest that burn serum induces PKG activation and the stress variety of filamentous actin in the vascular endothelial cells, which probably contributes to the endothelial hyperpermeability after burn shock. [
ABSTRACT
AIM: To examine the changes in immune cells which might be involved in systemic immune dysfunction after severe burns, we detected the sequence of expressed sequence tag in lymphocytes and monocytes of F344 rats post-burn. METHODS: Two pairs of primers were designed depending on the sequence of AI764697.1. SMART RACE technology was employed for amplification of whole sequence. Furthermore, the amplified sequence was testified by Northern blot. RESULTS: A 592bp sequence, which was testified by Northern blot, was suceessfally obtained in our experiments. This product was accepted by GenBank and its accession number is AF244895. CONCLUSION: A cDNA whole sequence in immune cells of F344 rats after severe burns was amplified successfully. More research work should be done to identify the resource, location in genome and function of this product.
ABSTRACT
AIM: To identify the effects of nitric oxide synthase (NOS) inhibitor on NO production, expression of NOS and mean artery pressure (MAP) in rats with severe burns. METHODS: After administration of non-selective NOS inhibitor, L-NAME, and selective inducible NOS (iNOS) inhibitor, aminoguanidine (AG), to rats with severe burns, levels of NO - 2/NO - 3 in blood, mRNA expression of nerve NOS (nNOS) in lung and duodenum, MAP in each group were calculated. RESULTS: Levels of NO - 2/NO - 3 in blood of rats increased significantly post burn, which could be inhibited by L-NAME and AG, especially by L-NAME. Expression of nNOS mRNA in lung and duodenum of rats increased post burn, which could be enhanced by AG and L-NAME. MAP of rats decreased gradually post burn and administration of AG could slow down this process significantly. CONCLUSION: cNOS and iNOS could play different roles in the pathophysiology of burn shock. Over-expression of iNOS could be closely related to the pathogenesis of burn shock.