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缩窄修复术后矛盾性高血压的发病机制。

Pathogenesis of paradoxical hypertension after coarctation repair.

作者信息

Fox S, Pierce W S, Waldhausen J A

出版信息

Ann Thorac Surg. 1980 Feb;29(2):135-41. doi: 10.1016/s0003-4975(10)61651-7.

DOI:10.1016/s0003-4975(10)61651-7
PMID:6986855
Abstract

A recent review of 25 patients who had repair of coarctation of the aorta at the Milton S. Hershey Medical Center revealed a 56% incidence of paradoxical hypertension in the immediate postoperative period. Analysis of results from recent animal experiments helped us to formulate a logical explanation of the pathogenesis of this hypertension. Stimulation of sympathetic nerve fibers located between the media and adventitia of the aortic isthmus has two effects, both of which result in hypertension. The first effect is release of norepinephrine and consequential rise in systemic blood pressure. Second, this spinal reflex directly stimulates the juxtaglomerular cells to release renin and cause additional hypertension. An additional effect of this increased renin production might be the shunting of blood from mesenteric arteries, thus causing the abdominal symptoms of so-called post-coarctectomy syndrome. The inability of some patients to adapt to this spinal reflex may be related to the age of the patient when the coarctation was repaired. This probably explains the high incidence of persistent hypertension in patients who undergo coarctation repair after adolescence.

摘要

最近对在米尔顿·S·赫尔希医疗中心接受主动脉缩窄修复手术的25例患者进行的一项回顾显示,术后即刻矛盾性高血压的发生率为56%。对近期动物实验结果的分析有助于我们对这种高血压的发病机制作出合理的解释。刺激位于主动脉峡部中膜与外膜之间的交感神经纤维会产生两种效应,这两种效应都会导致高血压。第一种效应是去甲肾上腺素的释放以及随之而来的全身血压升高。第二种效应是这种脊髓反射直接刺激球旁细胞释放肾素并导致进一步的高血压。肾素分泌增加的另一个效应可能是血液从肠系膜动脉分流,从而导致所谓的缩窄切除术后综合征的腹部症状。一些患者无法适应这种脊髓反射可能与修复缩窄时患者的年龄有关。这可能解释了青春期后接受缩窄修复手术的患者中持续性高血压的高发生率。

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Pathogenesis of paradoxical hypertension after coarctation repair.缩窄修复术后矛盾性高血压的发病机制。
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