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凝血酶诱导血管内凝血后肾血管阻力的变化:血小板和纤维蛋白栓子的作用

Renal vascular resistance changes following thrombin-induced intravascular coagulation: role of platelet and fibrin emboli.

作者信息

Hoie J

出版信息

Acta Chir Scand. 1975;141(3):167-72.

PMID:1166740
Abstract

The renal vasculature in the dog reacts to thrombin-induced intravascular coagulation with increasedd resistance. A constant rate infusion of 75 NIHu thrombin/kg b.w. reduced renal blood flow by approximately 55% in 30 min. Renal blood flow had almost regained preinfusion values within 30 min after the end of the infusion. Marked reduction in renal blood flow was not associated with increment of renal regional radioactivity in dogs pretreated with Cr-51 labeled platelets. The renal a-v difference in platelet counts did not contrast with other regions subjected to identical doses of thrombin. It is therefore unlikely that the flow changes are caused by vascular blockage by platelets. The flow decrease was accompanied by increase renal radioactivity in dogs pretreated with I-125 fibrinogen. This may imply renal accumulation of fibrin with obstruction to flow. Substantial renal blood flow reduction occurred with no or insignificant consumption of fibrinogen or changes in renal radioactivity after defibrinogenation. It is concluded that thrombin also induces a humoral vasoconstriction in the kidney.

摘要

犬的肾血管系统对凝血酶诱导的血管内凝血反应为阻力增加。以75 NIHu凝血酶/千克体重的恒定速率输注,30分钟内肾血流量减少约55%。输注结束后30分钟内,肾血流量几乎恢复到输注前的值。在用Cr-51标记血小板预处理的犬中,肾血流量的显著减少与肾局部放射性的增加无关。肾血小板计数的动静脉差异与接受相同剂量凝血酶的其他区域无差异。因此,血流变化不太可能是由血小板阻塞血管引起的。在用I-125纤维蛋白原预处理的犬中,血流减少伴随着肾放射性增加。这可能意味着纤维蛋白在肾内积聚并阻塞血流。去纤维蛋白原后,肾血流量大幅减少,同时纤维蛋白原消耗极少或无消耗,肾放射性也无变化。结论是,凝血酶也可诱导肾脏发生体液性血管收缩。

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Renal vascular resistance changes following thrombin-induced intravascular coagulation: role of platelet and fibrin emboli.凝血酶诱导血管内凝血后肾血管阻力的变化:血小板和纤维蛋白栓子的作用
Acta Chir Scand. 1975;141(3):167-72.
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