首页> 外文期刊>Cryobiology: International Journal of Low Temperature Biology and Medicine >The beneficial hemodynamic effects of afterload reduction by sodium nitroprusside during rewarming from experimental hypothermia
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The beneficial hemodynamic effects of afterload reduction by sodium nitroprusside during rewarming from experimental hypothermia

机译:实验性低温再次硝酸钠钠在硝酸钠中减少的有益血流动力学效应

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Abstract Background Rewarming from hypothermia is associated with depressed cardiac function, known as hypothermia-induced cardiac dysfunction (HCD), and increased systemic vascular resistance (SVR). Previous studies on pharmacological treatment of HCD have demonstrated beneficial effects when using drugs with the combined effects; cardiac inotropic support and peripheral vasodilation. The presented study aims to investigate the isolated effects of arterial dilatation on cardiac functional variables during rewarming from hypothermia using sodium nitroprusside (SNP). Methods We utilized a rat model designed to induce HCD following 4?h?at 15?°C and rewarming. To study effects on left ventricular (LV) functional variables in response to afterload reduction by SNP during rewarming a conductance catheter was used. Index of LV contractility, preload recruitable stroke work (PRSW), was obtained with inferior vena cava occlusions at 37?°C before and after hypothermia. Pressure signals from a catheter in the left femoral artery was used to pharmacologically adjust SVR. Results After rewarming both animal groups showed significant reduction in both SV and CO as a manifestation of HCD. However, compared to saline controls, SV and CO in SNP-treated animals increased significantly during rewarming in response to afterload reduction displayed as reduced SVR, mean arterial- and end-systolic pressures. The cardiac contractility variable PRSW was equally reduced after rewarming in both groups. Conclusion When rewarming the present model of HCD a significant increase in SVR takes place. In this context, pharmacologic intervention aimed at reducing SVR show clear positive results on CO and SV. However, a reduction in SVR alone is not sufficient to fully alleviate CO during HCD, and indicate the need of additional inotropic support.
机译:从体温过低的抽象背景与抑郁的心脏功能有关,称为低温诱导的心脏功能障碍(HCD),以及增加的全身血管阻力(SVR)。以前对HCD的药理治疗的研究表明,使用药物具有综合影响时的有益效果;心脏矫形载体和外周血管舒张。本研究旨在探讨使用硝普钠(SNP)从低温抑制过程中动脉扩张对心功能变量的分离效应。方法采用旨在诱导4℃的大鼠模型4?H〜15?°C和重新处理。为了响应于复活期间通过SNP在复活期间响应于SNP的后载减少而研究对左心室(LV)功能变量的效果。 LV收缩性指数,预加载令核卒中工作(PRSW)是在体温过低37℃下的37℃下的下腔静脉闭塞获得。左侧股动脉中导管的压力信号用于药理学上调节SVR。结果在再次手术后,动物组在SV和CO中表现出显着减少,作为HCD的表现。然而,与盐水对照相比,SNP处理的动物中的SV和CO在再次化过程中随着SVR的降低,平均动脉和末端 - 收缩压而显示的后载减少,SNP处理的动物中的SV和CO显着增加。在两个组中重新处理后,心脏收缩性变量PRSW同样减少。结论当复活时,HCD的目前模型发生了显着增加的SVR。在这种情况下,旨在减少SVR的药理学介入显示CO和SV的明显阳性结果。然而,单独的SVR的降低不足以在HCD期间完全缓解CO,并表明需要额外的渗透性载体。

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