Gathiram P, Wells M T, Brock-Utne J G, Wessels B C, Gaffin S L
Department of Physiology, University of Durban-Westville, South Africa.
J Clin Pathol. 1987 Nov;40(11):1364-8. doi: 10.1136/jcp.40.11.1364.
Four anaesthetised monkeys were given oral kanamycin (15 mg 1 kg 12 hourly) over five consecutive days before being heat stressed. Four other anaesthetised monkeys served as controls. The plasma lipopolysaccharide concentration in control primates increased initially from 0.044 (SEM 0.004) ng/ml to 0.062 (0.006) ng/ml as the rectal temperature increased from 37.5 to 39.5 degrees C. A second increase in lipopolysaccharides started at 42 degrees C and reached 0.308 (0.038) ng/ml (p less than 0.01) at 44.5 degrees C. Before heat stress the plasma lipopolysaccharide concentration in the primates who had been pretreated with kanamycin was 0.007 (0.006) ng/ml, and despite heating these animals to 44.5 degrees C no increase in plasma lipopolysaccharide concentrations were seen in this group. The cardiovascular variable during heat stress were more unstable in the control group and began to deteriorate at a lower temperature than in the group receiving antibiotic. These data suggest that the increased plasma lipopolysaccharide concentration during heat stress originates mainly from the gut.
四只麻醉的猴子在受热应激前连续五天口服卡那霉素（每千克体重15毫克，每12小时一次）。另外四只麻醉的猴子作为对照。随着直肠温度从37.5摄氏度升至39.5摄氏度，对照灵长类动物的血浆脂多糖浓度最初从0.044（标准误0.004）纳克/毫升升至0.062（0.006）纳克/毫升。脂多糖的第二次升高始于42摄氏度，并在44.5摄氏度时达到0.308（0.038）纳克/毫升（p<0.01）。在热应激前，用卡那霉素预处理的灵长类动物的血浆脂多糖浓度为0.007（0.006）纳克/毫升，尽管将这些动物加热到44.5摄氏度，但该组血浆脂多糖浓度未见升高。热应激期间对照组的心血管变量更不稳定，且在比接受抗生素组更低的温度下就开始恶化。这些数据表明，热应激期间血浆脂多糖浓度升高主要源于肠道。
