液体复苏对感染性休克狒狒模型心功能变化的影响。

I C Dormehl, J Kilian, J P Pretorius, A L van Gelder, N Hugo
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引用次数: 0

摘要

剧烈的心脏容量损失伴随着动脉压和肺毛细血管楔压(PCWP)的下降被发现是狒狒细菌性感染性休克模型的特征。血管张力的丧失和可能的血管液体泄漏被认为是促成因素。为了证明这一假设,我们计划用感染性休克的狒狒模型进行实验,并增加了一项流体管理方案,其中肺楔压保持在7 +/- 2毫米汞柱。6只狒狒作为自己的对照。通过液体负荷提高PCWP导致左心室容积下降的衰减,导致卒中容积(SV)的较小下降和左心室射血分数的较小增加。动脉压的下降仍然存在,因此左心室中风功反映了SV的下降。EDV/PCWP的依从性保持不变。因此,液体负荷虽然不能使血流动力学参数正常化,但导致心功能的一些测量的较小变化和改善。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The effect of fluid resuscitation on cardiac function changes monitored by radionuclide ventriculography in the septic shock baboon model.

Dramatic cardiac volume losses accompanied by a drop in arterial pressure and in pulmonary capillary wedge pressure (PCWP) were found to characterise the baboon model in bacterial septic shock. Loss of vascular tone and a probable vascular fluid leak were regarded as contributing factors. To prove this hypothesis an experiment was planned with the baboon model in septic shock, and an added protocol for fluid administration whereby the pulmonary wedge pressure was kept at 7 +/- 2 mm Hg. The six baboons served as their own controls. Raising PCWP by means of fluid loading resulted in an attenuation of the drop in left ventricular volumes, to a smaller decrease in stroke volume (SV) and smaller increases in left ventricular ejection fraction. The drop in arterial pressure remained and left ventricular stroke work therefore reflected the decrease in SV. Compliance as by EDV/PCWP remained unchanged. Fluid loading therefore, although not normalising the haemodynamic parameters, led to smaller changes and an improvement in some measures of cardiac function.

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