Abu-Zidan F M, Walther S, Lennquist S
Department of Surgery, University Hospital, Linköping Sweden.
Circ Shock. 1994 Nov;44(3):148-53.
Endotoxemia was induced by intravenous infusion of Escherichia coli endotoxin in 18 anesthetized pigs in a dose of 36 micrograms/kg/hr. Nine pigs were pretreated with BB-882, a novel platelet-activating factor (PAF) antagonist, 33 mg/kg/hr, starting 30 min before endotoxin, and nine pigs received a similar volume of vehicle. Normotension was maintained with intravenous crystalloid resuscitation. Six pigs received only BB-882 and served as controls. Endotoxemia induced an acute transient 300% increase in pulmonary vascular resistance, identical in both groups. The initial increase was followed by a second, more gradual, rise in resistance, which was significantly attenuated by BB-882 (P < 0.01, repeated measurements ANOVA). Endotoxin-induced arterial deoxygenation and fall in lung/thorax compliance was not significantly altered by BB-882. Hematocrit was less in endotoxic pigs receiving BB-882 (P < 0.02). There were no significant changes compared to baseline in the control group. The results indicate that PAF is a minor determinant of early pulmonary dysfunction in nonhypotensive porcine endotoxemia.
通过以36微克/千克/小时的剂量对18头麻醉猪静脉输注大肠杆菌内毒素来诱导内毒素血症。9头猪在给予内毒素前30分钟开始，以33毫克/千克/小时的剂量用新型血小板活化因子（PAF）拮抗剂BB - 882进行预处理，另外9头猪给予等量的赋形剂。通过静脉晶体复苏维持正常血压。6头猪仅接受BB - 882并作为对照。内毒素血症导致肺血管阻力急性短暂增加300%，两组情况相同。最初的增加之后是第二次更缓慢的阻力上升，BB - 882使其显著减弱（P < 0.01，重复测量方差分析）。BB - 882对内毒素诱导的动脉脱氧和肺/胸顺应性下降没有显著改变。接受BB - 882的内毒素血症猪的血细胞比容较低（P < 0.02）。与对照组的基线相比没有显著变化。结果表明，PAF是无低血压的猪内毒素血症早期肺功能障碍的次要决定因素。
