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The first part: the rat cardiopulmonary resuscitation model Objective: To establish a stable model of cardiopulmonary resuscitation in rats. Methods: 66 adult SD rats, random number divided into normal control group of eight, sham-operated group (n = 8), recovery group (n = 50). Recovery group from the external jugular vein bolus injection of potassium chloride-induced cardiac arrest, chest compressions and mechanical ventilation continued after 5min. Sham-operated group only intubation and intravascular catheters. Monitoring vital signs, record restoration of spontaneous circulation, neurological function recovery after 24h, 72h, and the observed normal control group, sham group and recovery after 1h, 12h, 72h brain tissue pathological changes each time point. Results: The rats immediately after the injection of potassium chloride circulatory arrest, restoration of spontaneous circulation (343.6 ± 120.2), restoration of spontaneous circulation was 80% (40/50), 24h survival rate of 76%, 72h survival 74%. Recovery after 24h neurological score (64.73 ± 1.66), 72h (73.19 ± 1.33) min. Recovery 1h brain tissue after hypoxic-ischemic injury heaviest, 24h, followed by gradual improvement, 72h. Conclusion: The model is stable and reliable, easy to operate and easy recovery, the most obvious improvement is the use of intubation to minimize tissue damage and effects on the body, and thus more suitable for post-cerebral resuscitation CPR research. Part II: spermidine / spermine-N1-acetyltransferase 2, HIF-1alpha in rat brain tissue after cardiopulmonary resuscitation in the dynamic changes of purpose: study after cardiopulmonary resuscitation in rat brain tissue spermidine / amine -N1-acetyltransferase 2 (spermidine/spermine-N1-acetyltransferase2, SSAT2) and hypoxia-inducible factor-1α (hypoxia inducible factor 1 alpha, HIF-1α) expression of dynamic variation, analyzing the correlation of the two. Methods: 88 SD rats were randomly digital divided into normal control group, sham group and cardiopulmonary resuscitation. Sham operation group and cardiopulmonary resuscitation 1,8,24,48,72 H 5 group is further divided into subgroups, each subgroup 8. Using RT-PCR and Western blot methods were used to detect the the brain tissue HIF-1alpha mRNA and HIF-1α, SSAT2 protein expression. Results: the expression of SSAT2 recovery was significantly lower 1h (0.314 ± 0.027, P lt; 0.01) was the lowest, followed by a downward trend (P lt; 0.01) gradually weakened to 72 h (0.731 ± 0.024, P gt; 0.05) restored to the level of the normal control group (0.736 ± 0.020), the expression of the sham-operated group SSAT2 compared with the control group did not change significantly (P gt; 0.05) HIF-1alpha mRNA expression in the recovery after 1h (0.245 ± 0.021, P lt; 0.05) decreased 8 h (0.430 ± 0.019, P lt; 0.05) significantly enhanced, 24h (0.387 ± 0.018, P lt; 0.05) 48h (0.385 ± 0.019, P lt; 0.05) slightly increased to 72h, down to the level of the normal control group (0.343 ± 0.022); HIF-1alpha protein expression levels after recovery 1h (0.755 ± 0.012, P lt; 0.01 ) was significantly higher, and then tended to increase gradually slow down (P lt; 0.01), increased only slightly to 72 h (0.033 ± 0.002, P lt; 0.01), while in the normal control group and sham operation group failed to detect HIF-1alpha expression. SSAT2 expression of HIF-1alpha expression in recovery within 72h after negative correlation (r = -0.945, P lt; 0.001), SSAT2 expression of HIF-1alpha mRNA expression in the recovery after 8 to 48 h showed a negative correlation (r = -0.614, P = 0.001). Conclusion: within 72 hours after cardiopulmonary resuscitation in rat brain tissue HIF-1alpha protein expression increased and tended to increase gradually weakened decline in SSAT2 expression and the downward trend is slowing down; recovery after 8 to 48 hours when the increase in the expression of HIF-1alpha mRNA and increasing trend is slowing. SSAT2 HIF-1α, HIF-1αmRNA expression was negatively correlated with the opposite trend, suggesting SSAT2 HIF-1α, HIF-1αmRNA may play a negative regulatory role.
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