高温复合脂多糖应激大鼠平均动脉压的变化规律

CHANGES OF MEAN ARTERIAL PRESSURE IN LPS-HEAT CO-STRESSED RATS.

目的：监测并探讨高温（HS）复合细菌脂多糖（LPS）应激大鼠平均动脉压的动态变化特点，为进一步探讨重度热射病的发病机制奠定基础。方法：雄性SPF级Wistar大鼠随机分为：常温生理盐水组（C组）、高温生理盐水组（H组）、常温LPS组（L组）、高温LPS组（HL组）。持续监测动物平均动脉压（MAP）的动态变化。结果：L组动物于致伤50～60min时MAP出现一过性显著性降低（P〈0．05，与C组比较）；H组、HL组动物MAP出现先升后降，变化趋势，于应激60min时MAP即显著上升（P〈0．01，与C组/L组比较），于应激100～110min分别达峰值（132．6±3．4）mmHg、（128．4±2．7）mmHg，迅速出现循环衰竭，分别降至（67．2±418）mmHg、（49．0±3．5）mmHg；H组、HL组动物MAP差异有统计学意义（P〈0．01）。结论：高温与LPS复合应激动物感染性休克的程度显著加重。

Objective： To investigate the effects of co-exposure of LPS and heat on mean arterial pressure in rats. Methods： Male pathogen- free Wister rats were randomly assigned to the following groups： saline- injected normothermic control （C - Group）, saline- injected heat exposed （H- Group）, LPS- injected normothermic control （L - Group）, LPS-injected heat exposed （HL-Group）. Mean arterial pressure （MAP） was continually monitored. Result： There was a significant and transient difference in the values of MAP between L- Group and C-Group at 5060min time point （P〈 0.05, L-Group vs. C-Group）. The rats in H- Group and HL- Group displayed significantly high values of MAP since 60min time point and reached their peaks at 100～110 min time point （ 132.6 ± 3.4） mm Hg and （ 128.4 ± 2.7） mm Hg respectively, then decreased rapidly to （67.2 ± 4.8） mm Hg and （49.0 ± 3.5） mm Hg respectively. There was a significant difference in the values of MAP between HL - Group and H - Group. Conclusion： These data may suggest that co-exposure of LPS and heat primes the rat to advance and augment septic shock.