目前,有确凿证据表明,细菌产物能引起“败血病休克”综合征的各种血液动力学临床表现。虽然,正是内毒素——革兰氏阴性菌外膜中复合脂多糖的脂蛋白A被认为是败血病休克最常见的致病因素,但是败血病休克不仅限于革兰氏阴性菌感染。的确,抗生素的应用(或滥用)有助于无病因的菌血症感染由以前的革兰氏阳性球菌占优势转变为目前更为常见的革兰氏阴性杆菌。据说,这些药物的使用增加了内毒素休克的发病率。抗生素促进内毒素释放的直接证据是在用大肠杆菌实验感染兔的研究中获得的。给动物用庆大霉素或安慰剂,通过鲎(Limalus)试验定期测定血浆游离内毒素水平。鲎试验基于 At present, there is strong evidence that bacterial products can cause various hemodynamic manifestations of “septic shock” syndrome. Although lipoprotein A, which is the complex lipopolysaccharide in the outer membrane of endotoxin-Gram-negative bacteria, is considered to be the most common causative agent of septic shock, septic shock is not limited to Gram-negative bacterial infections . Indeed, the use of antibiotics (or misuse) helps the etiological bacteremia infection shift from predominant Gram-positive cocci to more common Gram-negative bacilli. It is said that the use of these drugs increases the incidence of endotoxic shock. Direct evidence that antibiotics promote endotoxin release was obtained in a study of rabbits infected with E. coli. Animals were given gentamicin or placebo and plasma levels of free endotoxin were measured periodically by the Limalus test.鲎 test based on