ABSTRACT
Objective To observe the changes of potassium ion (K+), lactic acid (Lac) and glucose (Glu) in swine with traumatic hemorrhagic shock (THS) inside the dry-heat environment and to explore its possible mechanism. Methods A total of 40 local Landrace piglets were randomly(random number) divided equally into 4 groups: the normal temperature sham operation group (NS), the normal temperature traumatic hemorrhagic shock group (NTHS), the dry-heat sham operation group (DS group) and the dry-heat traumatic hemorrhagic shock group (DTHS). The experiment was carried out in the artifi cia climate cabin simulated the special environment of northwest of China. After exposed to their respective environment[dry-heat environment: (40.5±0.5), plus(10±2)% humidity; normal temperature environment: (25±0.5), plus(35±5)% humidity] for 3 h. Laparotomy were performed in swine of all groups, and then splenectomy and partial hepatectomy were performed only in NTHS and DTHS. The process of exsanguination from the external iliac artery was established to make the MAP reaching to 40-50 mmHg, and thus the traumatic hemorrhagic shock model of swine was successfully made. Blood samples were collected from external iliac artery at different intervals including the time just after exposure for 3 h and the successful establishment of traumatic hemorrhagic shock model (0 h) and then every 30 min after 0 h, serum levels of K+, Lac and Glu were detected. The features of varied serum K+, Lac and Glu were observed in each group. All data were statistically analyzed using One-way ANOVA and Pearson correlation analysis. Results After exposed , the level of serum K+inside the dry-heat environment was higher than that of swine inside the normal temperature group ( P<0.01), however the Glu level was lower in the swine inside dry-heat environment than that of swine inside the normal temperature ( P<0.01).The level of serum K+and Lac of DTHS group were rapidly increased from the establishment of the model to the death in about 3 h, while those of NTHS group were increased slowly. The level of K+and Lac were positively correlated in the two groups amd the correlation coeffi cient were rDTHS=0.927 (P<0.01) and rNTHS=0.539 (P<0.01),respectively. The level of Glu was progressively decrease in DTHS group, while in NTHS group, it was not noticeable. The level of K+and Glu were negatively correlated in the two group, the correlation coeffi cient were rDTHS=-0.804 (P<0.01) and rNTHS=0.420 (P<0.01),respectively. Conclusions The changes of serum K+, Lac and Glu occurred sooner and more obvious in traumatic hemorrhagic shock models inside dry heat environment (DTHS) group than those in NTHS group. The level of serum K+positively correlated with Lac, however, negatively correlated with Glu, which suggested that hyperkalemia and acidosis should be paid more attention to the treatment of traumatic hemorrhagic shock inside the dry heat environment, and the hypoglycemia should be treated at the same time.
ABSTRACT
OBJECTIVE: The authors investigated whether rotenone induces cellular death also in non-dopaminergic neurons and high concentration of potassium ion can show protective effect for non-dopaminergic neuron in case of rotenone-induced cytotoxicity. METHODS: Neuro 2A cells was treated with rotenone, and their survival as well as cell death mechanism was estimated using 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium(MTT) assay, Lactate dehydrogenase(LDH) release assay, fluorescence microscopy, and agarose gel electrophoresis. The changes in rotenone-treated cells was also studied after co-treatment of 50mM KCl. And the protective effect of KCl was evaluated by mitochondrial membrane potential assay and compared with the effects of various antioxidants. RESULTS: Neuro 2A cells treated with rotenone underwent apoptotic death showing chromosome condensation and fragmentation as well as DNA laddering. Co-incubation of neuro 2A cells with 50mM KCl prevented it from the cytotoxicity induced by rotenone. Intracellular accumulation of reactive oxygen species(ROS) resulting by rotenone were significantly reduced by 50mM KCl. Potassium exhibited significantly similar potency compared to the antioxidants. CONCLUSION: The present findings showed that potassium attenuated rotenone-induced cytotoxicity, intracellular accumulation of ROS, and fragmentation of DNA in Neuro 2A cells. These findings suggest the therapeutic potential of potassium ion in neuronal apoptosis, but the practical application of high concentration of potassium ion remains to be settled.