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牛急性巴贝斯虫(=阿根廷巴贝斯虫)感染期间激肽、激肽原和激肽酶水平

Kinin, kininogen and kininase levels during acute Babesia bovis (= B. argentina) infection of cattle.

作者信息

Wright I G

出版信息

Br J Pharmacol. 1977 Dec;61(4):567-72. doi: 10.1111/j.1476-5381.1977.tb07549.x.

Abstract
  1. Kinin levels began rising on day 3 after infection of cattle with Babesia bovis (= B. argentina) and attained a maximum value of 98% above preinfection levels by day 7. 2. Kininogen levels began falling on day 3 and reached minimum levels of 83% below preinfection levels on day 8. 3. Changes in both kinin and kininogen levels on day 3 coincided with the detection of low levels of parasites, and with a fall in packed cell volume. 4. Plasma kininase levels rose significantly 6 to 9 days after infection. Preparations of lysed and sonicated uninfected and infected red cells contained kininase activity, the respective red cell preparations being 23.9 and 11.4 times more active per mg protein than uninfected red cell preparations. The effect of pH, and the inhibitors disodium edetate, 1,10 phenanthroline and aprotinin on normal and infected plasma and on the various red cell preparations suggested that the rise in plasma kininase levels during infection was probably at least partly due to parasite products. 5. These results are discussed in relation to previous data showing that both kallikrein activation and the onset of hypotension also occur on or about day 3.
摘要
  1. 用牛巴贝斯虫(=阿根廷巴贝斯虫)感染牛后,激肽水平在第3天开始上升,到第7天达到比感染前水平高98%的最大值。2. 激肽原水平在第3天开始下降,在第8天降至比感染前水平低83%的最低水平。3. 第3天激肽和激肽原水平的变化与低水平寄生虫的检测以及血细胞比容的下降同时发生。4. 感染后6至9天血浆激肽酶水平显著升高。裂解和超声处理的未感染和感染红细胞制剂含有激肽酶活性,每毫克蛋白质的相应红细胞制剂比未感染红细胞制剂的活性分别高23.9倍和11.4倍。pH值以及抑制剂依地酸二钠、1,10-菲啰啉和抑肽酶对正常和感染血浆以及各种红细胞制剂的影响表明,感染期间血浆激肽酶水平的升高可能至少部分归因于寄生虫产物。5. 结合先前的数据讨论了这些结果,先前的数据表明激肽释放酶激活和低血压发作也在第3天左右发生。

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本文引用的文献

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In vitro studies on the mechanism of kinin formation by trypanosomes.锥虫形成激肽机制的体外研究。
Br J Pharmacol. 1968 Nov;34(3):598-603. doi: 10.1111/j.1476-5381.1968.tb08488.x.
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Immune reactions and kinin formation in chronic trypanosomiasis.慢性锥虫病中的免疫反应与激肽形成
Br J Pharmacol Chemother. 1968 Mar;32(3):493-504. doi: 10.1111/j.1476-5381.1968.tb00450.x.

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