The role of the reticulo-endothelial system in hemorrhagic shock.
The role of the reticulo-endothelial system in hemorrhagic shock.
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DOI：
10.1084/jem.110.4.547
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发表时间：
1959-10-01
期刊：
影响因子：
--
通讯作者：
SCHWEINBURG FB
中科院分区：
文献类型：
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作者：
FINE J;RUTENBURG S;SCHWEINBURG FB
Thorotrast对RES的“阻断”降低了兔和狗对失血性休克的耐受性，使可逆程度的失血性休克变为不可逆。这不仅在正常家兔中是真实的，而且在通过产生对内毒素的抗性而抵抗出血性休克的家兔中也是真实的。用thorotrast预处理然后进行失血性休克的家兔在死亡时显示出出血性病变和Shwartzman反应特征性的肾皮质坏死，此外还有肠壁内出血，这是死于出血性或内毒素休克的动物的特征。通过预先给予氮芥消除Shwartzman反应并不能预防内毒素血症或休克死亡。通过预先重复给予Thorotrast，使其对Thorotrast的抵抗力比正常家兔更强，对内毒素的抵抗力也比正常家兔更强，并且在通常致命的出血性休克暴露中存活。在给药后的最初几个小时内，thorotrast不仅诱导了对内毒素和失血性休克的过度脆弱性，而且还诱导了额外小剂量的thorotrast。此外，在thorotrast后不久通过灌胃给予不可吸收的抗生素产生与这些其他药剂相同的病变;即内毒素休克、Shwartzman反应和死亡。这些数据表明，thorotrast诱导的病变是由内毒素产生的，损伤或阻塞的RES不能阻止内毒素。这些家兔血液中内毒素的存在通过该血液对试验受体的致死作用来指示。上述观察结果不适用于肠道植物群不含大肠菌群的家兔。超过80%的这种兔子对通常致命的失血性休克具有抵抗力，它们逃脱了通常剂量的thorotrast造成的伤害。然而，如果给予大剂量的thorotrast，他们确实会发生内毒素休克并死亡。这些数据表明，无大肠菌兔并非完全无内毒素。(In普通环境动物不能避免吞食内毒素和大肠菌群。在无大肠菌群的家兔中不存在Shwartzman反应，表明该反应需要来自肠内细菌的内毒素参与。无大肠菌兔中无内毒素休克，表明大肠菌群的内毒素参与了携带大肠菌群的兔的休克和死亡。最后，在具有正常植物群的家兔中，二苯丁胺对Shwartzman反应和内毒素休克及死亡的预防表明，肾上腺素能活性在这两种现象中起着不可或缺的作用。上述数据为以下论点提供了强有力的支持：当RES被任何药剂严重禁用时，正常并持续从肠道进入循环的内毒素将产生内毒素休克和死亡。
"Blockade" of the RES by thorotrast so lowered the tolerance of hemorrhagic shock in rabbits and dogs that a reversible degree of hemorrhagic shock became irreversible. This was true not only in normal rabbits, but in rabbits made resistant to hemorrhagic shock by producing resistance to endotoxins. Rabbits which had been pretreated with thorotrast and then subjected to hemorrhagic shock displayed at death the hemorrhagic lesions and the renal cortical necrosis characteristic of the Shwartzman reaction, in addition to the intramural hemorrhages in the gut which are characteristic of animals dying of hemorrhagic or of endotoxic shock. Elimination of the Shwartzman reaction by the prior administration of nitrogen mustard did not prevent the endotoxemia or the death in shock. Rabbits made more resistant to thorotrast than normal rabbits by prior repeated administration of this substance were also more resistant than normal rabbits to endotoxin, and survived an ordinarily lethal exposure to hemorrhagic shock. During the first few hours after its administration thorotrast induced excessive vulnerability not only to endotoxin and to hemorrhagic shock, but also to an additional small dose of thorotrast. Moreover, a non-absorbable antibiotic given by gavage shortly after thorotrast produced the same lesions as these other agents; i.e. endotoxic shock, the Shwartzman reaction, and death. These data indicate that the lesions induced by thorotrast are produced by endotoxins which the injured or blockaded RES cannot inactivate. The presence of endotoxins in the blood of these rabbits was indicated by the lethal effect of this blood in test recipients. The foregoing observations did not apply to rabbits with an intestinal flora free of coliform bacteria. Over 80 per cent of such rabbits were resistant to an ordinarily lethal exposure to hemorrhagic shock, and they escaped the damage caused by the usual doses of thorotrast. They did, however, develop endotoxic shock and die if given a large dose of thorotrast. These data were taken to indicate that coliform-free rabbits are not entirely free of endotoxins. (In the ordinary environment animals cannot avoid swallowing endotoxin and coliform bacteria.) The absence of the Shwartzman reaction in the coliform-free rabbits is taken to signify that this reaction requires the participation of the endotoxins derived from the intraintestinal bacteria. The absence of endotoxic shock in the coliform-free rabbits is taken to signify that the endotoxins of the coliform bacteria are involved in the shock and death of the coliform-bearing rabbits. Finally the prevention by dibenamine of both the Shwartzman reaction and endotoxic shock and death in rabbits with a normal flora demonstrates that adrenergic activity plays an indispensable role in both phenomena. The foregoing data provide strong support for the thesis that when the RES is severely disabled by any agent, endotoxins which normally and continuously enter the circulation from the gut will produce endotoxic shock and death.