| Objective To study the change of immune ingredients on heat exposed rats in the thermal enviroment and the resistive effect of glycine on rat's endotoxemia led by heat exposure, enrich the theory of heat stroke and establish bases for its prevention and treatment.Methods 1.108 SD rats were randomly divided into 3 groups: normal control group, heat stress group and heat acclimatization group. Each group exposed to different enviroment for 2 hours. And then, TNF RIA kit, NO kit, immunohistoch~mistry and image analysis were used to study the change of TNF, NO in serum and DC in mesenteric lymph node respectively. In the end, we described the fluctuant curves of the changes.2. 24 SD Rats were divided into three groups, two groups exposed in thermal enviroment (Td 41 ?0.5 0C, Tw35 ?1 ~C , relative humidity60-66%) were given glycine (G) and 0.9%saline (NS) respectively, normal control (NC) group was exposed to room temperature. Time of exposure was 80mm. Heat shock time, survival time (interval between onset of heat shock and death), the rectal temperature (Tr) -. heart rate (HR) ~. mean arterial pressure(MAP) before and after heat exposure were measured in different groups, and then compare the value among different groups.3. 108 SD rats, grouping method was the same as ?? thermal enviroment (Td 39 ?0.5 0C, Tw3 5? ~C relative humidity6o-66%), time of exposure was l2Omin.And then study the change of concentration of TNIF in different groups.Results 1. Change of TNF: After heat stress, TNF in serum increased and reached the peak point at 4h(12363r0.9lnglml) .Then it declined, got the least point at 24h.The concentration of TNF in heat stress group was lower than that of normal control group (P<0.05) . Concentration of TNF in heat acclimatization group under the same heat-exposed conditions fluctuated around the level being higher than that of normal group, it reached the peak-4-point at 4h and was still higher than the conceniration of TNF in heat stressgroup. (Prt0. 05) 2. Change of NO: After heat exposed 2 hours, NO inserum represented a short time decline. During point 2h-4h, it increasedobviously, then dropd again. And reached the normal level at 24h.Conceniration of NO was higher than that of normal grouP at each time-point(except 4h, 12h, P<0.05).3.Change of DC: In HS grouP a-nd HA group,number of DC increased after 2-hour heat exposure. It reached the peak pointat 8h, l2.5MP in HS grouP, and presented an obvious trend of increasing anddeclining. Number of DC in HA grouP rised too, but did not fluctUateobviously, the highest value was 6.70/HP Comparing with normal controlgrouP, number of DC in HS grouP and HA group increased obviously (pr0.0l ). DC was cloud -like, centra1ized and presented pseudopod surroundingthe lymph node after heat stress. 4. Change of physioIogical paremeterafter usage of G: Duration from heat stress to heat shock and survival time,in G grouP, were longer than that in NS group (Pr0.01 ). During initialst&ges while exposed to thermal enviromeni, the rectal temPeratue(Tr),mean arterial pressure(MAP) and heaIt rates of G group presented no \,different from NS grouP (P>0.05 ), but they were all higher than that of '-norma1 grouP (Pwt0.01 ). Heart rate and rectal temperatUIe of G grouP were lf:obviously lower than that of NS group at the end of heat exposure. MAP ofNS grouP declined to 9.3 Kpa, rats presented heat shock at 80min. ThoughMAP declined either in G group, it was still higher than that of NS grouP (P<0.05 ) .5. Effect of G on TNF: ThF in serum of G grouP was lower thanthat of NS grouP at 0h, 2h, 4h, even more it was lower tha-n that of normalgroup. Concentration of TNF increased at 4h-8h, the highest value was6.N.tw. And then, concentration of TNF was at low leve1.Conclusion l.Endotoxemia of Rats suffered from heat-exposure cancause the increasing of T'NF. Concentration of NO declines at Frst and thenrises. DC's sharp in thermal enviroment changed obviously, its numberincrea...
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