Gathiram P, Gaffin S L, Brock-Utne J G, Wells M T
Department of Physiology, University of Durban-Westville, South Africa.
Aviat Space Environ Med. 1988 Feb;59(2):142-5.
We previously found that lipopolysaccharides (LPS) leak from the gut lumen into the hepatic portal vein during heat stroke. Furthermore, we found that prophylactic corticosteroid administration could prevent a rise in plasma LPS concentration in superior mesenteric artery occlusion shock. In this study, we found that treatment prior to heat-stress with corticosteroids could prevent any rise in plasma LPS concentration in heat-stressed primates. Two groups of primates, one of which received a prophylactic dose of methylprednisolone sodium succinate (MPSS) (n = 4) were subjected to heat-stress (41 +/- 0.3 degrees C). Their arterial blood pressure, heart rate and rectal temperature (Tr) were continuously recorded. In the untreated control group (n = 8), the plasma LPS concentration tended to increase slowly at a Tr of 41.5 degrees C from an initial 0.06 +/- 0.013 ng.ml-1. Above a Tr of 43 degrees C, the plasma LPS level rose rapidly until at a Tr of 44.4 +/- 0.1 degrees C, the mean LPS level was 0.315 +/- 0.03 ng.ml-1 (p less than 0.001). Prophylactic treatment with MPSS suppressed the increase in plasma LPS levels to 0.066 +/- 0.01 ng.ml-1 before heat-stress and 0.03 +/- 0.01 ng.ml-1 at Tr 44.4 degrees C just before primate demise. The mean arterial pressure of the control group was lower than the treated group for any given Tr; between Tr 42-43 degrees this difference was significant (p less than 0.05). Moreover, the cardiovascular parameters began to deteriorate at a lower Tr in the control group.
我们之前发现，在中暑期间脂多糖（LPS）会从肠腔渗漏至肝门静脉。此外，我们还发现预防性给予皮质类固醇可预防肠系膜上动脉闭塞性休克时血浆LPS浓度升高。在本研究中，我们发现热应激前用皮质类固醇进行治疗可预防热应激灵长类动物血浆LPS浓度升高。两组灵长类动物，其中一组接受预防性剂量的琥珀酸钠甲泼尼龙（MPSS）（n = 4），接受热应激（41±0.3℃）。持续记录它们的动脉血压、心率和直肠温度（Tr）。在未治疗的对照组（n = 8）中，血浆LPS浓度在Tr为41.5℃时从初始的0.06±0.013 ng/ml开始缓慢升高。在Tr高于43℃时，血浆LPS水平迅速上升，直到Tr为44.4±0.1℃时，平均LPS水平为0.315±0.03 ng/ml（p<0.001）。MPSS预防性治疗可将热应激前血浆LPS水平升高抑制至0.066±0.01 ng/ml，在灵长类动物死亡前Tr为44.4℃时降至0.03±0.01 ng/ml。在任何给定的Tr下，对照组的平均动脉压均低于治疗组；在Tr为42 - 43℃之间，这种差异具有统计学意义（p<0.05）。此外，对照组心血管参数在较低的Tr时就开始恶化。
