Mileski W J, Winn R K, Harlan J M, Rice C L
Department of Surgery, University of Washington School of Medicine, Seattle 98104.
J Appl Physiol (1985). 1992 Sep;73(3):1146-9. doi: 10.1152/jappl.1992.73.3.1146.
The immunoinflammatory response following trauma and hemorrhage may predispose to the development of sepsis and multiple-organ failure syndrome. Cardiac output (CO), arterial pressure, arterial PO2, and pulmonary permeability index were measured. We examined the sensitivity of rabbits to infusions of lipopolysaccharide (LPS) after hemorrhagic shock. Shock was produced by reducing CO to 40% of baseline for 90 min, followed by resuscitation with shed blood and then with lactated Ringer solution to maintain CO near baseline. Animals were assigned to three groups: 1) hemorrhagic shock only, 2) LPS only, and 3) hemorrhagic shock + LPS. Groups 1 and 3 were subjected to hemorrhagic shock on day 1. Escherichia coli LPS was infused (1.0 microgram/kg i.v.) into groups 2 and 3 on day 2. Fluid resuscitation with lactated Ringer solution was continued in an effort to maintain CO at baseline. Five hours after LPS infusion, 125I-albumin was injected intravenously, and rabbits were killed 1 h later for measurement of pulmonary permeability index. LPS infusion after shock (group 3) caused significant decreases in CO, arterial pressure, and PO2 and an increase in pulmonary permeability. These changes were not seen in the groups 1 and 2. We conclude that hemorrhagic shock and resuscitation result in a proinflammatory state, leading to increased sensitivity to subsequent exposure to LPS.
创伤和出血后的免疫炎症反应可能易导致脓毒症和多器官功能衰竭综合征的发生。测量了心输出量（CO）、动脉压、动脉血氧分压（PO2）和肺通透性指数。我们研究了失血性休克后家兔对脂多糖（LPS）输注的敏感性。通过将CO降至基线的40%并维持90分钟来制造休克，随后用自体血复苏，然后用乳酸林格液复苏以维持CO接近基线水平。动物被分为三组：1）仅失血性休克组，2）仅LPS组，3）失血性休克 + LPS组。第1组和第3组在第1天接受失血性休克。第2组和第3组在第2天静脉输注大肠杆菌LPS（1.0微克/千克）。继续用乳酸林格液进行液体复苏以维持CO在基线水平。LPS输注后5小时，静脉注射125I-白蛋白，1小时后处死家兔以测量肺通透性指数。休克后输注LPS（第3组）导致CO、动脉压和PO2显著降低以及肺通透性增加。第1组和第2组未出现这些变化。我们得出结论，失血性休克和复苏导致促炎状态，导致对随后接触LPS的敏感性增加。
