Suppr超能文献

沙伊氏氯白血病发病机制中红细胞生成潜力的评估。

Evaluation of erythropoietic potential during pathogenesis of the Shay chloroleukemia.

作者信息

Derelanko M J, Khouri J A, Meagher R C, LoBue J, Gordon A S

出版信息

J Surg Oncol. 1980;15(2):139-46. doi: 10.1002/jso.2930150206.

Abstract

To evaluate the erythropoietic potential of rats during pathogenesis of Shay chloroleukemia (SCL), SCL animals were exposed to hypoxia initiated within two hours postinduction of SCL. Increases in hematocrit (HCT) occurred in both SCL and nonleukemic controls during the first seven days of exposure. This was followed by declines in HCT in hypoxic SCL rats similar to that observed in nonhypoxic SCL animals. HCT of nonleukemic controls remained elevated throughout hypoxic exposure. Results suggested that in SCL, erythropoietic homeostatic response mechanisms are functional prior to terminal phases of this disease, whereas anemia-producing mechanisms exceed maximum erythropoietic capacity of these animals during later stages of SCL. The HCT of most SCL rats exposed to hypoxia did not fall below 40% before death. This was in contrast to nonhypoxic SCL animals, which became severely anemic in terminal stages. No survival value was observed despite maintenance of red cell mass at or above normal. The pathogenesis of this leukemia was independent of the leukemic animal's erythropoietic potential.

摘要

为了评估大鼠在沙伊氏绿色白血病(SCL)发病过程中的红细胞生成潜力,在诱导SCL后两小时内,将SCL动物置于低氧环境中。在暴露的前七天,SCL动物和非白血病对照组的血细胞比容(HCT)均升高。随后,低氧SCL大鼠的HCT下降,这与非低氧SCL动物中观察到的情况相似。非白血病对照组的HCT在整个低氧暴露期间均保持升高。结果表明,在SCL中,红细胞生成稳态反应机制在该疾病的终末期之前是有功能的,而在SCL后期,贫血产生机制超过了这些动物的最大红细胞生成能力。大多数暴露于低氧环境的SCL大鼠在死亡前HCT未降至40%以下。这与非低氧SCL动物形成对比,后者在终末期会出现严重贫血。尽管红细胞量维持在正常或以上水平,但未观察到生存价值。这种白血病的发病机制与白血病动物的红细胞生成潜力无关。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验