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肾衰竭中的肾心相互作用(作者译)

[Reno-cardiac interactions in kidney failure (author's transl)].

作者信息

Kramer P, Schmidt-Lauber M, Langenheim N, Zwehl W, Sold G, Luig H, Matthaei D, Gröne H J, Henning H V, Scheler F

出版信息

Klin Wochenschr. 1980 Oct 1;58(19):1043-50. doi: 10.1007/BF01476875.

Abstract

The high incidence of cardiac complications in endstage renal failure is not only related to the chronic pressure load of the left ventricle, although the proportion of patients with elevated blood pressure increases from 53 to 81% as reno-parenchymal disease progresses. Other factors as anemia, hyperparathyroidism, autonomic neuropathy and retention of electrolytes, metabolic products of toxins may cause damage to the heart. It is a matter of discussion whether uremia itself causes cardiomyopathy. Findings of a reduced Ca++-uptake during beta-adrenergic stimulation and a reduced reaction of (Na+, K+)-ATPase to digitalis suggest a basic change of myocardial membrane metabolism. Retention of an "endogenous digitalis" could help to explain some contradictory results.

摘要

终末期肾衰竭中心脏并发症的高发生率不仅与左心室的慢性压力负荷有关,尽管随着肾实质疾病的进展,血压升高的患者比例从53%增至81%。其他因素如贫血、甲状旁腺功能亢进、自主神经病变以及电解质、毒素代谢产物的潴留都可能对心脏造成损害。尿毒症本身是否会导致心肌病仍存在争议。β-肾上腺素能刺激期间Ca++摄取减少以及(Na +,K +)-ATP酶对洋地黄反应降低的结果提示心肌膜代谢存在基本改变。“内源性洋地黄”的潴留有助于解释一些相互矛盾的结果。

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