Lang C H, Bagby G J, Nowotny A, Spitzer J J
Circ Shock. 1985;17(4):301-11.
Although the polysaccharide portion of bacterial endotoxins (ET) and other components of the bacterial cell wall are known to possess biological activity, the toxic effects produced by ET have been attributed mostly to the lipid-A component. The present study examined the influence of selected gram-negative cell wall components on in vivo carbohydrate homeostasis. Chronically catheterized conscious rats were injected with either ET, lipid A, the White polysaccharide supernatant (WPS-S; polysaccharide-rich and lipid-A-free) or the WPS-precipitate (WPS-P; rich in cell wall components and lipid-A-free) at sublethal doses of 100, 10, and 1 microgram/100 g. The acute hypotensive response to ET and lipid A were similar, while the WPS-P induced a smaller reduction in pressure. Endotoxin, lipid A, or the WPS-P (100 and 10 micrograms) all produced hyperglycemia. Hyperlactacidemia was evident in rats receiving ET, lipid A, and WPS-P; ET-treated animals exhibited the highest lactate concentrations. At the highest doses used, these three fractions increased the rate of glucose appearance. The polysaccharide-rich WPS-supernatant elicited no significant alterations in any of the variables studied. These results indicate that cell wall components of gram-negative bacteria, other than the lipid A of endotoxin, induce changes in carbohydrate metabolism that are similar to those produced by the toxic, lipid-A component of endotoxin.
尽管已知细菌内毒素（ET）的多糖部分及细菌细胞壁的其他成分具有生物活性，但ET产生的毒性作用大多归因于脂质A成分。本研究检测了所选革兰氏阴性菌细胞壁成分对体内碳水化合物稳态的影响。对长期通过导管插管的清醒大鼠，以100、10和1微克/100克的亚致死剂量注射ET、脂质A、白色多糖上清液（WPS-S；富含多糖且不含脂质A）或WPS沉淀物（WPS-P；富含细胞壁成分且不含脂质A）。ET和脂质A引起的急性降压反应相似，而WPS-P引起的血压下降较小。内毒素、脂质A或WPS-P（100和10微克）均导致高血糖。接受ET、脂质A和WPS-P的大鼠出现明显的高乳酸血症；接受ET治疗的动物乳酸浓度最高。在所使用的最高剂量下，这三个组分均提高了葡萄糖生成速率。富含多糖的WPS上清液在所研究的任何变量中均未引起显著变化。这些结果表明，革兰氏阴性菌的细胞壁成分，除了内毒素的脂质A外，也会诱导碳水化合物代谢发生变化，这些变化与内毒素有毒的脂质A成分所产生的变化相似。
