Kaplan J E
Adv Shock Res. 1979;2:73-81.
Numerous studies have demonstrated that reticuloendothelial system (RES) depression induced by colloid blockade increases susceptibility to circulatory shock following trauma and sepsis. Recent data have suggested that this may relate to the failure of the RES to clear potentially embolic material derived from activation of the hemostatic system. The present study thus compared the hypotensive response precipitated by trauma or sepsis with that resulting from induction of intravascular coagulation. Mean arterial blood pressure (MABP) was monitored for 120 minutes after sublethal NCD trauma and after intra-aortic injection of live E coli (approximately 10(10) organisms per rat), E coli endotoxin (0.1 mg/100 gm), or bovine thrombin (10 units/100 gm) in 400-500 gm rats 30 minutes after RE blockade (50 mg/100 gm gelatinized lipid colloid) or saline injection. All rats were anesthetized with sodium pentobarbital. No hypotension was observed in blockaded control rats. After trauma, MABP decreased by 20 minutes after injury and recovered to normal levels by 1 hour post-trauma. MABP decreased in blockaded rats after trauma and remained diminished through 2 hours. After live E coli endotoxin or thrombin, both the normal and the blockaded groups underwent an initial hypotension of similar magnitude. A second period of hypotension was much more pronounced in the RE-blockaded animals. Reduced MABP persisted in these animals through 2 hours. These data indicate that RE blockade enhances the hypotensive response to intravascular coagulation and that resulting from trauma or sepsis. This effect was especially apparent during the second phase of hypotension during sepsis and intravascular coagulation. It was suggested that the RES manifests some protective effect against the agents inducing this secondary hypotensive response.
大量研究表明，胶体阻断诱导的网状内皮系统（RES）抑制会增加创伤和脓毒症后发生循环性休克的易感性。最近的数据表明，这可能与RES无法清除源自止血系统激活产生的潜在栓塞物质有关。因此，本研究比较了创伤或脓毒症引发的低血压反应与血管内凝血诱导产生的低血压反应。在体重400 - 500克的大鼠中，在RES阻断（50毫克/100克明胶化脂质胶体）或注射生理盐水30分钟后，给予亚致死性非控制性失血性创伤（NCD创伤），或经主动脉注射活大肠杆菌（每只大鼠约10¹⁰个菌）、大肠杆菌内毒素（0.1毫克/100克）或牛凝血酶（10单位/100克），随后监测平均动脉血压（MABP）120分钟。所有大鼠均用戊巴比妥钠麻醉。在阻断对照大鼠中未观察到低血压。创伤后，MABP在受伤后20分钟下降，并在创伤后1小时恢复到正常水平。创伤后，阻断组大鼠的MABP下降，并在2小时内持续降低。在注射活大肠杆菌内毒素或凝血酶后，正常组和阻断组均出现了幅度相似的初始低血压。在RES阻断的动物中，第二个低血压期更为明显。这些动物的MABP降低持续了2小时。这些数据表明，RES阻断增强了对血管内凝血以及创伤或脓毒症所致低血压反应。在脓毒症和血管内凝血的低血压第二阶段，这种作用尤为明显。有人提出，RES对诱导这种继发性低血压反应的因素具有一定的保护作用。
