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不稳定型心绞痛患者白细胞及激肽释放酶-激肽系统的激活

Activation of leukocytes and of the kallikrein-kinin system in patients with unstable angina pectoris.

作者信息

Hoffmeister H M, Beyer M E, Engel Z, Heller W

机构信息

Medical Department III, University of Tübingen, Germany.

出版信息

Clin Cardiol. 1994 Jan;17(1):27-30. doi: 10.1002/clc.4960170106.

Abstract

We investigated the leucocyte-elastase and the activity of the kallikrein system including kinin precursors and plasma inhibition levels in 14 patients with unstable angina pectoris (normal or only slightly elevated creatinine kinase levels; no transmural myocardial infarction) and compared them with 10 controls. Leucocyte-elastase levels and activity of the kallikrein system were significantly elevated in unstable angina pectoris. The bradykinin precursor high-molecular-weight kininogen was markedly decreased to 79 +/- 16% indicating kinin generation. Except for a slight decrease in the beta factor XIIa inhibition, we observed no abnormalities in the plasma kallikrein inhibition or in the antithrombin III levels in patients with unstable angina pectoris. The findings indicate a significant activation of the plasma kallikrein-kinin system, which is not associated with a considerable reduction in the plasma inhibitor levels. Kinin generation might influence vascular tone and leucocyte function and thus be involved in the pathophysiologic alterations occurring in patients with recurrent angina at rest.

摘要

我们研究了14例不稳定型心绞痛患者(肌酐激酶水平正常或仅略有升高;无透壁性心肌梗死)的白细胞弹性蛋白酶以及激肽释放酶系统的活性,包括激肽前体和血浆抑制水平,并将其与10名对照者进行比较。不稳定型心绞痛患者的白细胞弹性蛋白酶水平和激肽释放酶系统活性显著升高。缓激肽前体高分子量激肽原明显降至79±16%,表明有激肽生成。除β因子XIIa抑制略有降低外,我们未观察到不稳定型心绞痛患者的血浆激肽释放酶抑制或抗凝血酶III水平有异常。这些发现表明血浆激肽释放酶-激肽系统有显著激活,这与血浆抑制剂水平的显著降低无关。激肽生成可能影响血管张力和白细胞功能,从而参与静息性复发性心绞痛患者发生的病理生理改变。

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