Plasma immunoreactive endothelin, but not thrombomodulin, is increased in patients with essential hypertension and ischemic heart disease.

Plasma immunoreactive endothelin, but not thrombomodulin, is increased in patients with essential hypertension and ischemic heart disease.
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原发性高血压和缺血性心脏病患者的血浆免疫反应性内皮素升高,但血栓调节蛋白不升高。

DOI:
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发表时间:
1991
影响因子:
3
通讯作者:
K. Ohsumi
K. Ohsumi
中科院分区:
医学4区
文献类型:
--
作者:
M. Naruse;M. Kawana;S. Hifumi;K. Naruse;I. Yoshihara;T. Oka;Y. Kato;C. Monzen;F. Kurimoto;K. Ohsumi

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为了确定血管内皮细胞在心血管疾病中的作用,我们测定了高血压(EH)和缺血性心脏病患者血浆中两种内皮衍生物质--内皮素(ET)和血栓调节蛋白(TM)的水平。提取后用放射免疫法测定血浆ET含量。用酶免疫法测定血浆TM水平。EH合并靶器官损害、血管痉挛心绞痛(VSA)、急性心肌梗死(AMI)患者血浆ET水平显著升高,尤以心源性休克患者更为显著。EH患者血浆ET水平与血肌酐浓度之间存在微弱但显著的相关性。在冠脉痉挛之前,VSA患者的血浆ET水平就已经升高,而在冠脉痉挛期间,血浆ET水平没有进一步升高。而EH和VSA患者的血浆TM水平与正常人相比差异无统计学意义。这些结果表明,ET在EH和缺血性心脏病的病理生理过程中起重要作用,血浆ET的升高不能简单地归因于损伤内皮细胞的多肽泄漏。
To ascertain an involvement of vascular endothelial cells in cardiovascular disease, we have determined plasma levels of two endothelium-derived substances, endothelin (ET) and thrombomodulin (TM), in essential hypertension (EH) and ischemic heart disease. Plasma ET was determined by radioimmunoassay (RIA) after extraction. Plasma TM levels were determined by enzymunoimmunoassay. Plasma ET levels were significantly elevated in patients with EH involving target organ damage, vasospastic angina pectoris (VSA), and acute myocardial infarction (AMI), especially in those associated with cardiogenic shock. There was a weak but significant correlation between plasma ET levels and serum creatinine concentration in patients with EH. Plasma ET levels were elevated even before the coronary spasm in patients with VSA, whereas they did not show any further increase during the spasm. In contrast, plasma TM levels in patients with EH and VSA did not show a significant difference from that in normal subjects. These results suggest that ET plays an important role in the pathophysiology of EH and ischemic heart disease, and also that increases in plasma ET cannot be simply attributed to a leakage of the peptide from the injured endothelial cells.