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Effect of volume loading on the Frank–Starling relation during reductions in central blood volume in heat-stressed humans

机译:在热应激的人中,中央血容量减少时,容量负荷对Frank-Starling关系的影响

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摘要

During reductions in central blood volume while heat stressed, a greater decrease in stroke volume (SV) for a similar decrease in ventricular filling pressure, compared to normothermia, suggests that the heart is operating on a steeper portion of a Frank–Starling curve. If so, volume loading of heat-stressed individuals would shift the operating point to a flatter portion of the heat stress Frank–Starling curve thereby attenuating the reduction in SV during subsequent decreases in central blood volume. To investigate this hypothesis, right heart catheterization was performed in eight males from whom pulmonary capillary wedge pressure (PCWP), central venous pressure and SV (via thermodilution) were obtained while central blood volume was reduced via lower-body negative pressure (LBNP) during normothermia, whole-body heating (increase in blood temperature ∼1°C), and during whole-body heating after intravascular volume expansion. Volume expansion was accomplished by administration of a combination of a synthetic colloid (HES 130/0.4, Voluven) and saline. Before LBNP, SV was not affected by heating (122 ± 30 ml; mean ±s.d.) compared to normothermia (110 ± 20 ml; P= 0.06). However, subsequent volume loading increased SV to 143 ± 29 ml (P= 0.003). LBNP provoked a larger decrease in SV relative to the decrease in PCWP during heating (8.6 ± 1.9 ml mmHg−1) compared to normothermia (4.5 ± 3.0 ml mmHg−1, P= 0.02). After volume loading while heat stressed, the reduction in the SV to PCWP ratio during LBNP was comparable to that observed during normothermia (4.8 ± 2.3 ml mmHg−1; P= 0.78). These data support the hypothesis that a Frank–Starling mechanism contributes to compromised blood pressure control during simulated haemorrhage in heat-stressed individuals, and extend those findings by showing that volume infusion corrects this deficit by shifting the operating point to a flatter portion of the heat stress Frank–Starling curve.
机译:与正常体温相比,在受到热应激的情况下,中央血液量减少时,中风量(SV)的下降幅度较大,而心室充盈压也有类似下降,这表明心脏在Frank-Starling曲线的较陡峭部分上运转。如果这样的话,热应激个体的体负荷将使工作点移动到热应激Frank-Starling曲线的较平坦部分,从而在随后的中心血容量减少期间减弱SV的降低。为了研究该假设,对八名男性进行了右心导管检查,从中获得肺毛细血管楔压(PCWP),中心静脉压和SV(通过热稀释),而在此期间通过下体负压(LBNP)降低中心血容量体温正常,全身加热(血液温度升高约1°C)以及血管内体积膨胀后的全身加热。通过施用合成胶体(HES 130 / 0.4,Voluven)和盐水的组合来实现体积膨胀。与正常体温(110±20 ml; P = 0.06)相比,在LBNP之前,SV不受加热(122±30 ml;平均值±s.d.)的影响。但是,随后的体积加载将SV增加到143±29 ml(P = 0.003)。与常温加热(4.5±3.0 ml mmHg-1,P = 0.02)相比,LBNP引起的相对于加热期间PCWP的降低(8.6±1.9 ml mmHg-1)SV的降低更大。在承受热应力的体积加载后,LBNP期间SV与PCWP的比率的降低与正常温度下的观察结果相当(4.8±2.3 ml mmHg-1; P = 0.78)。这些数据支持以下假设:在热应激个体的模拟出血期间,Frank–Starling机制有助于降低血压控制,并通过显示体积输注将操作点移至热量的较平坦部分来纠正这一缺陷,从而扩展了这些发现。强调弗兰克-史达琳曲线。

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