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Objective: To observe a high-temperature environment scalded rats peripheral blood T lymphocyte subsets, NK cell activity and inflammatory mediators IL-6, IL-10, TNF-alpha changes in hot climates scalded rats immune function. Methods: 72 healthy SD rats, male and female, body weight (200 ± 20) g were randomly divided into four groups: group A (room temperature feeding burns keeping at room temperature, n = 18), group B (breeding at room temperature burns high temperature keeping, n = 18) and group C (high REVISION clothing burn keepers at room temperature, n = 18) and D group (REVISION suit burn high temperature keepers, n = 18). After experimental animals acclimatized for a week, the A and B group continued at room temperature keeping 10 days, C, D group in the artificial climate box [temperature (38 ± 1) ° C; relative humidity of (55 ± 5)%] 1 h / d, 10d continuously observe and record the rectal temperature changes in the rat basal body temperature and heat exposure, high temperature acclimatization to be rats. The 11th day of each rat hair removal, anesthesia, resulting in 30% TBSA III degree burns, burns A, C group continued to room temperature, feeding, B, D group at high temperatures feeding. Rats were observed living conditions 1, 3 and 7 days after injury from each of six under sterile conditions in vivo to take inferior vena venous 5 ml of 2 ml of EDTA-tubes evacuation flow cytometry chamber to detect T lymphocyte subsets, NK cell activity and CD25 T lymphocytes, 3ml centrifugal ELISA for detection of inflammatory mediators IL-6, IL-10, TNF-alpha. Results: 1. Study suit rats before and after exposure to heat rectal temperature changes: the rats in the high temperature environment, heat rectal temperature was significantly higher than the pre-heating, the difference was statistically significant (P lt; 0.05 or P LT; 0.01) ; the 9th day of rectal temperature decreased to heat exposure level, the difference was not significant (P GT and heat exposure; 0.05), Description rats have adapted to the high temperature environment. (2) the observation of the survival of rats in each group: A, C, D rats during the experiment no deaths occurred in group B after injury to high temperature environment keeping the majority of rats after 120 min shortness of breath, irritability, such as performance . 4h after death, the day after the injury has died 15, 2d to hurt all died. (3) comparison of the immune function of rats in each group: (1) A, group B rats immune activity; group B and group A, CD3 changes little (P gt; 0.05), CD4 T lymphocytes, CD4 / CD8 CD25 T lymphocytes, NK cell activity was significantly decreased (P lt; 0.05 or P LT; 0.01), CD8 T lymphocytes was significantly higher (P lt; 0.01). (2) A, C group after injury at each time point immune activity in rats; group C compared with group A, at each time point CD3 little change after injury (P gt; 0.05), one day after the injury CD8 T lymphocytes was significantly higher (P lt; 0.01) 7 days after injury CD4 T lymphocytes decreased significantly (P lt; 0.05), 1,7 days after injury CD4 / CD8, CD25 T lymphocytes, NK cell activity was significantly decreased (P lt; 0.05 or P lt; 0.01) (3) C, D group after injury at each time point immune activity in rats: D and C groups after injury at each time point CD3, CD4 / CD8, CD25 T lymphocytes were significantly lower, CD8 T lymphocytes increased (P lt; 0.05 or P LT; 0.01). 1 day after injury CD4 T lymphocytes decreased significantly (P lt; 0.05), 1,3 days after the injury, NK cell activity was significantly decreased (P lt; 0.05 or P LT; 0.01) (4), one day after the injury of Group D rats immune activity; D group compared with group B, CD4 T lymphocytes, CD4 / CD8, CD25 T lymphocytes, little change in the activity of NK cells (P gt; 0.05) CD3, CD8 T lymphocytes was significantly reduced (P lt; 0.05 or P LT; 0.01). 4 each rat IL-6, IL-10, TNF-alpha inflammatory mediators comparison: (1) group B compared with group A, IL-6, IL-10, TNF-α was significantly higher (P lt ; 0.01). (2) C in group A compared to one day after the injury, IL-6, IL-10, TNF-alpha was significantly higher (P lt; 0.01), 3,7 days after injury, no significant change (P GT; 0.05) . (3) D group compared with C group after injury, at each time point, IL-6, IL-10, TNF-alpha was significantly higher (P lt; 0.01) (4) D group compared with group B, one day after the injury, IL-6, IL-10, TNF-alpha was significantly lower (P lt; 0.01). Conclusion: heat stress in the pre-injury and post-injury serious damage to the cellular immune function of rats to expand its inflammatory response. 2 pre-injury heat acclimatization can reduce such damage, improve the ability of rat high temperature. High burn multiple stress than burn single factor on the cellular immune function of rats damage and inflammatory response is even more serious.
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