[Study on the changes in the distribution and chemical states of the hepatic intra-and extra-cellular sodium ion in the rats with severe burns at early stage].

OBJECTIVE: To investigate the changes in the distribution and chemical states of the hepatic intra- and extra-cellular sodium ion in the rats with severe burns, so as to provide guidance for fluid resuscitation at early postburn stage. METHODS: Nineteen adult male Sprague-Dawley (SD) rats were employed in the study and were randomly divided into control (n = 12) and burn (n = 7) groups. The changes in the longitudinal (T1) and transverse (T2) relaxation times of hepatic intra-cellular and extra-cellular sodium in the two groups were studied with 23Na NMR spectroscopy and a shift reagent. RESULTS: After infusion of the shift reagent,the extra-cellular sodium content in rat liver decreased by 17%, with obvious increase in fast T2 component (P < 0.01), indicating an increase in the fraction of Na+ binding sites in the extra-cellular space. The characteristics of relaxation of intra-cellular sodium remained unchanged despite a 57% increment in intra-cellular sodium content. CONCLUSION: The deficiency of sodium as a permeable molecule might be related to the postburn movement of hypertonic sodium from extra-cellular to intra-cellular space. The results indicated that it is reasonable to administer high concentration of sodium in fluid resuscitation during the first 24 postburn hours.

[Role of p38 mitogen-activated protein kinase in the pathogenesis of stress ulcer].

OBJECTIVE: To determine whether the activation of p38 mitogen-activated protein kinase (MAPK) is involved in the pathogenesis of stress ulcer. METHODS: Model of stress ulcer was established with the treatment of rats with water-immersion restraint (WIR) stress. Ulcer index (UI) was macroscopically evaluated as a parameter of gastric mucosal lesions. Expression of phospho- and pan-p38 in gastric mucosa was detected using Western blot analysis. Tumor necrosis factor-alpha (TNF-alpha) and Interleukin 1beta (IL-1beta) gene expressions were analyzed by Northern blot analysis. As indicated in some experiments, rats were pretreated with intravenous injection of the specific p38 MAPK inhibitor CNI-1493 prior to WIR stress and then the changes of UI and TNF-alpha and IL-1beta mRNA expression were examined. RESULTS: The p38 MAPK was persistently activated in the gastric mucosa of rats with WIR stress, with maximal activation after 1 h of stress [(6.8 +/- 3.2) fold of baseline levels, P < 0.01]. Inhibition of p38 MAPK activation with CNI-1493 led to a marked decrease in UI in WIR stress rats. Similarly, the increased gene expression of proinflammatory cytokines TNF-alpha and IL-1beta in gastric mucosa induced by WIR stress were significantly diminished by p38 MAPK inhibition. CONCLUSION: p38 MAPK might have an important role in the pathogenesis of stress ulcer.