PATHO-PHYSIOLOGY OF SHOCK AND HEMORRHAGE IN A FULMINATING VIRAL-INFECTION (EBOLA)
PATHO-PHYSIOLOGY OF SHOCK AND HEMORRHAGE IN A FULMINATING VIRAL-INFECTION (EBOLA)
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DOI：
10.1093/infdis/152.5.887
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发表时间：
1985-01-01
影响因子：
6.4
通讯作者：
SIMPSON, DIH
中科院分区：
文献类型：
--
作者：
FISHERHOCH, SP;PLATT, GS;SIMPSON, DIH
在实验感染埃博拉病毒期间，对11只恒河猴进行了集中监测。最早出现的异常是明显的嗜中性粒细胞增多伴左移和淋巴细胞减少，在第4天时具有统计学意义（分别为P <0.02和P <0.01）。到第4天，血小板计数的福尔斯下降没有统计学意义，而体外血小板聚集明显受到抑制，迅速进展到最严重疾病时完全失败。血小板内蛋白研究表明，该事件是体内活化和脱粒的结果。凝血级联缺陷主要在内在系统中，并且令人惊讶地温和，没有证据表明因子VII或VIII的选择性消耗或生产缺陷。当检查可能由非特异性免疫应答间接介导的内皮损伤的可能性时，药物治疗的猴子体重减轻不太严重，并且所有猴子都有可检测到的血浆前列环素代谢物，但存活率没有改善。
Eleven rhesus monkeys were monitored intensively during experimental infection with Ebola virus. Prominent neutrophilia with left shift and lymphopenia were the earliest abnormalities and were statistically significant by day 4 (P < .02 and P < .01, respectively). By day 4 falls in platelet counts were not statistically significant, whereas in vitro platelet aggregation was markedly depressed, progressing rapidly to complete failure by the time of maximum illness. Intraplatelet protein studies suggested this event was the result of in vivo activation and degranulation. Coagulation cascade defects were mainly in the intrinsic system and were surprisingly mild, with no evidence of selective consumption or production deficit of factor VII or VIII. When the possibility of indirectly mediated damage to endothelium possibly by a nonspecific immune response was examined, weight loss were less severe in drug-treated monkeys, and all had detectable plasma prostacyclin metabolites, but there was no improvement in survival.