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1.
Chinese Journal of Burns ; (6): 326-328, 2005.
Article in Chinese | WPRIM | ID: wpr-312552

ABSTRACT

<p><b>OBJECTIVE</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>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.</p>


Subject(s)
Animals , Male , Rats , Burns , Metabolism , Cations , Metabolism , Extracellular Space , Metabolism , Hepatocytes , Metabolism , Rats, Sprague-Dawley , Sodium , Metabolism
2.
Chinese Journal of Surgery ; (12): 1284-1287, 2005.
Article in Chinese | WPRIM | ID: wpr-306120

ABSTRACT

<p><b>OBJECTIVE</b>To determine whether the activation of p38 mitogen-activated protein kinase (MAPK) is involved in the pathogenesis of stress ulcer.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>p38 MAPK might have an important role in the pathogenesis of stress ulcer.</p>


Subject(s)
Animals , Male , Rats , Disease Models, Animal , Interleukin-1 , Genetics , Rats, Sprague-Dawley , Stomach Ulcer , Genetics , Stress, Physiological , Tumor Necrosis Factor-alpha , Genetics , p38 Mitogen-Activated Protein Kinases , Metabolism , Physiology
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