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实验性慢性高血压对组织型纤溶酶原激活物活性、纤溶酶原激活物抑制及纤溶酶抑制的影响。

The effect of experimental chronic hypertension on tissue plasminogen activator activity, plasminogen activator inhibition and plasmin inhibition.

作者信息

Kokolis N, Ploumis T, Smokovitis A

机构信息

Department of Physiology, Faculty of Veterinary Medicine, Aristotelian University, Thessaloniki, Greece.

出版信息

Thromb Res. 1989 Nov 15;56(4):523-8. doi: 10.1016/0049-3848(89)90236-3.

DOI:10.1016/0049-3848(89)90236-3
PMID:2532794
Abstract

Chronic hypertension was induced in rats after partial nephrectomy. The systolic blood pressure was significantly elevated from the first week after nephrectomy to the end of the experimentation (8th week). Plasminogen activator activity (PAA) and plasminogen activator inhibition (PAI) showed a tissue- and time-dependent pattern of changes in some key organs compared to controls (sham-operated rats). Two weeks after nephrectomy (one week after the induction of hypertension) the PAA was markedly increased in lungs, heart and aorta. In aorta the PAA continued to be enhanced until the end of the experimentation (the 8th week after nephrectomy), while in heart and lungs the PAA returned to the normal eight weeks after nephrectomy. In vena cava, brain and liver no change in PAA was noticed compared to controls. Tissue PAI was mostly increased or unchanged, while tissue plasmin inhibition (PI) was unchanged. The differential response of PAA and PAI was varying not only from one organ to another or in the same organ at a given time but also in the same organ throughout experimentation. In a number of nephrectomized rats, however, hypertension was not induced. In these rats similar changes in tissue PAA and PAI were noted compared to hypertensive nephrectomized rats. Therefore, all the changes in the parameters studied should be due to the partial nephrectomy itself. In conclusion, experimentally induced chronic hypertension had not any effect on tissue PAA, PAI and PI.

摘要

大鼠肾部分切除术后诱发慢性高血压。从肾切除术后第一周直至实验结束(第8周),收缩压显著升高。与对照组(假手术大鼠)相比,纤溶酶原激活物活性(PAA)和纤溶酶原激活物抑制物(PAI)在一些关键器官呈现出组织和时间依赖性的变化模式。肾切除术后两周(高血压诱发一周后),肺、心脏和主动脉中的PAA显著增加。在主动脉中,PAA持续增强直至实验结束(肾切除术后第8周),而在心脏和肺中,PAA在肾切除术后八周恢复正常。与对照组相比,腔静脉、脑和肝脏中的PAA未发现变化。组织PAI大多增加或无变化,而组织纤溶抑制(PI)无变化。PAA和PAI的差异反应不仅在不同器官之间或同一器官在给定时间有所不同,而且在整个实验过程中同一器官内也有所不同。然而,在一些肾切除大鼠中未诱发高血压。与高血压肾切除大鼠相比,这些大鼠的组织PAA和PAI出现了类似变化。因此,所研究参数的所有变化应归因于肾部分切除术本身。总之,实验性诱发的慢性高血压对组织PAA、PAI和PI没有任何影响。

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