Merritt K, Galton M
J Bacteriol. 1967 Sep;94(3):590-6. doi: 10.1128/jb.94.3.590-596.1967.
The ability of bacterial endotoxin to produce the generalized Shwartzman reaction (GSR) in pregnant and nonpregnant hamsters was investigated. Endotoxins prepared from Escherichia coli O127:B8, Salmonella enteritidis, and S. typhosa 0-901 did not produce the GSR in nonpregnant hamsters. Injection of lead acetate did not make the hamsters susceptible to the GSR producing effects of endotoxin. Endotoxin administered to hamsters on either or both the 14th and 15th day of the 16-day gestation period caused fetal death, but did not provoke the GSR. The immunization of hamsters with boiled suspensions of gram-negative bacteria isolated from hamster feces did not protect against the GSR produced in pregnant hamsters by the injection of the antimitotic drug colchicine late in the gestation period. It appeared that colchicine was acting to produce the GSR by a mechanism other than the release of endogenous endotoxin through the damaged intestinal wall. Ascitic fluid, amniotic fluid, and serum obtained from pregnant hamsters developing the GSR after the administration of colchicine did not provoke the GSR in other pregnant hamsters.
研究了细菌内毒素在怀孕和未怀孕仓鼠中引发全身性施瓦茨曼反应(GSR)的能力。从大肠杆菌O127:B8、肠炎沙门氏菌和伤寒沙门氏菌0-901制备的内毒素在未怀孕仓鼠中不会引发GSR。注射醋酸铅不会使仓鼠对内毒素产生GSR的作用敏感。在16天妊娠期的第14天和第15天给仓鼠注射内毒素,会导致胎儿死亡,但不会引发GSR。用从仓鼠粪便中分离出的革兰氏阴性菌的煮沸悬液对仓鼠进行免疫,不能预防在妊娠期后期注射抗有丝分裂药物秋水仙碱后怀孕仓鼠产生的GSR。似乎秋水仙碱引发GSR的机制并非通过受损肠壁释放内源性内毒素。从注射秋水仙碱后发生GSR的怀孕仓鼠获得的腹水、羊水和血清,不会在其他怀孕仓鼠中引发GSR。