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先天性心脏缺陷手术后急性低心排血量综合征的治疗:依诺昔酮的价值

[Treatment of acute low cardiac output syndrome after surgery of congenital heart defects: value of enoximone].

作者信息

Schranz D, Bauer J, Wiemann J, Kühl G, Dapper F, Wippermann C F, Huth R, Oelert H

机构信息

Universitätskinderklinik Mainz.

出版信息

Z Kardiol. 1994;83 Suppl 2:83-9.

PMID:8091830
Abstract

Children undergoing cardiac surgery are at additional risk for postoperative low cardiac output syndrome (LCOS). Anticipation of the syndrome from preoperative hemodynamic condition, surgical procedure, and adverse intraoperative events is a key to successful postoperative management. Inotropic support is primarily based on catecholamines. However, uncoupling of human cardiac beta-adrenoceptors during cardiopulmonary bypass with cardioplegic cardiac arrest may be the reason why many patients respond only weakly to beta-adrenoceptor agonists. Phosphodiesterase (PDE) inhibitors act by reducing intracellular breakdown of cAMP, which is elevated independently from beta-receptors. The use of PDE-inhibitors might be advantageous in patients with uncoupled beta-adrenoceptors, as occurs after cardiopulmonary bypass. In addition, PDE-inhibitors can prevent further downregulation of the adrenoceptors due to avoiding prolonged therapy by beta-agonists. In this context, the addition of enoximone, a PDE-inhibitor, to adrenergic agents has been found useful in increasing cardiac output in children with catecholamine-resistant LCO, as well as in children with compensated hemodynamics during catecholamine therapy.

摘要

接受心脏手术的儿童术后发生低心排血量综合征(LCOS)的风险更高。根据术前血流动力学状况、手术过程及术中不良事件来预判该综合征是术后成功管理的关键。正性肌力支持主要基于儿茶酚胺。然而,在心肺转流期间使用心脏停搏液导致心脏停搏时,人体心脏β-肾上腺素能受体解偶联可能是许多患者对β-肾上腺素能受体激动剂反应微弱的原因。磷酸二酯酶(PDE)抑制剂通过减少细胞内cAMP的分解起作用,cAMP的升高独立于β受体。PDE抑制剂的使用可能对β受体解偶联的患者有利,如在心肺转流后出现的情况。此外,PDE抑制剂可避免因β激动剂长期治疗导致肾上腺素能受体进一步下调。在此背景下,已发现将PDE抑制剂依诺昔酮添加到肾上腺素能药物中,对于增加儿茶酚胺抵抗性LCO患儿的心排血量以及儿茶酚胺治疗期间血流动力学代偿良好的患儿的心排血量是有用的。

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