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1.
Chinese Journal of Traumatology ; (6): 38-42, 2006.
Article Dans Anglais | WPRIM | ID: wpr-280940

Résumé

<p><b>OBJECTIVE</b>To investigate the effects of seawater immersion on the function of myocardium and hepatocyte mitochondria in experimental hemorrhagic shock rats.</p><p><b>METHODS</b>Twenty-four male Wistar rats were divided into three groups (n=8 in each group): control group, HSL group (hemorrhagic shock group on land) and HSS group (hemorrhagic shock group in seawater). The hemodynamic parameters, activities of H(+)-ATPase (adenosinetriphosphatase), succinate dehydrogenase (SDH) and Ca(2+)-Mg(2+)-ATPase, the calcium contents in myocardium and hepatocyte mitochondria were measured and the changes of proton translocation across the inner mitochondrial membrane were analyzed.</p><p><b>RESULTS</b>The hemodynamic indexes and the activities of H+-ATPase, SDH, Ca(2+)-Mg(2+)-ATPase in HSS group were significantly lower than those in control group and HSL group (P<0.05). In HSS group the calcium levels in tissue and mitochondria of myocardium and hepatocyte were elevated significantly compared with control group and HSL group (P<0.05). There was no significant difference in proton translocation among three groups.</p><p><b>CONCLUSIONS</b>This investigation demonstrates that seawater immersion can aggravate the conditions of hemorrhagic shock rats.</p>


Sujets)
Animaux , Mâle , Rats , Calcium , Métabolisme , Immersion , Mitochondries du myocarde , Mitochondries du foie , Proton-Translocating ATPases , Métabolisme , Répartition aléatoire , Rat Wistar , Eau de mer , Choc hémorragique
2.
Chinese Journal of Traumatology ; (6): 293-297, 2006.
Article Dans Anglais | WPRIM | ID: wpr-280894

Résumé

<p><b>OBJECTIVE</b>To investigate the detrimental effects of hemorrhagic shock on the structure and function of mitochondria DNA (mtDNA) encoding cytochrome oxidase genes in intestinal epithelial cells.</p><p><b>METHODS</b>Wistar rats were used and divided into two groups: hemorrhagic shock group and control group. Hemorrhagic shock model of rats was utilized in this experiment. The mtDNA was extracted from the intestinal epithelial cells and amplified by polymerase chain reaction (PCR) with different primers of cytochrome oxidase (COX I, COX II and COX III). The products of PCR were directly sequenced.</p><p><b>RESULTS</b>Hemorrhagic shock could result in the point mutagenesis in mitochondrial genome encoding cytochrome oxidase (COX I and COX II). There were 4, 4, 22, 16, 35 point mutations in COX I from 5545 to 6838 bp in 5 shocked rats. There were five point mutations in COX II from 7191 to 7542 bp at the site of t7191c, t7212c, a7386g, a7483g, c7542g in 1 shocked rat. There was no mutation found in COX III.</p><p><b>CONCLUSIONS</b>Hemorrhagic shock could significantly induce the damage of the gene of cytochrome oxidase encoded by mtDNA.</p>


Sujets)
Animaux , Mâle , Rats , Séquence nucléotidique , ADN mitochondrial , Génétique , Complexe IV de la chaîne respiratoire , Génétique , Muqueuse intestinale , Mutation , Réaction de polymérisation en chaîne , Rat Wistar , Choc hémorragique , Génétique
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