CLINICAL SIGNS AND MORPHOLOGIC ABNORMALITIES IN GUNN RATS TREATED WITH SULFADIMETHOXINE
CLINICAL SIGNS AND MORPHOLOGIC ABNORMALITIES IN GUNN RATS TREATED WITH SULFADIMETHOXINE
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DOI：
10.1016/s0022-3476(69)80351-3
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发表时间：
1969-01-01
影响因子：
5.1
通讯作者：
JOHNSON, L
中科院分区：
文献类型：
--
作者：
SCHUTTA, HS;JOHNSON, L
在出生后18小时至33日龄期间给予磺胺二甲氧嘧啶治疗的大鼠出现急性神经症状，大脑黄染色增加。在4天至22天之间接受治疗的动物中，神经系统异常与血清胆红素水平成正比。出生后18至48小时治疗的动物比胆红素水平相似的老年动物出现更严重的症状，年龄超过22天的动物出现轻微但明确的神经症状。本研究证实了胆红素白蛋白结合作为高胆红素血症保护因子的重要性。我们的结论是，假设胆红素的血脑屏障来解释核黄疸是多余的，并且缺氧不是核黄疸发展的必要条件。在新生儿之后，胆红素可以进入中枢神经系统。本文讨论了磺胺类药物对Gunn大鼠在出生后2天毒性极大，而对28和33天的动物影响相对轻微的原因。这表明，核黄疸的特征性脑变黄在很大程度上可能是由脑血流的区域差异造成的。
Gunn rats treated with sulfadimethoxine between 18 hours after birth and 33 days of age developed acute neurologic signs and increased yellow staining of their brains. In animals treated between the ages of 4 and 22 days, the neurologic abnormalities were proportional to the serum bilirubin levels. Animals treated from 18 to 48 hours after birth develop more severe signs than older animals with similar bilirubin levels, and those older than 22 days develop mild but definite neurologic signs. This study confirms the importance of the albumin binding of bilirubin as a protective factor in hyperbilirubinemia. We conclude that it is superfluous to postulate a blood-brain barrier to bilirubin to explain kernicterus, and that anoxia is not essential for its development. Bilirubin has access to the central nervous system beyond the newborn period. The reasons for the extreme toxicity of sulfonamides to Gunn rats in the first 2 days of life and the relatively mild effects in animals treated at 28 and 33 days are discussed. It is suggested that the characteristic pattern of yellow discoloration of the brain in kernicterus could be largely accounted for by differences in regional cerebral blood flow.