Mechanisms for the control of local tissue blood flow during thermal interventions: influence of temperature-dependent ATP release from human blood and endothelial cells.
Mechanisms for the control of local tissue blood flow during thermal interventions: influence of temperature-dependent ATP release from human blood and endothelial cells.
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DOI：
10.1113/ep085910
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发表时间：
2017-02-01
影响因子：
2.7
通讯作者：
González-Alonso J
中科院分区：
文献类型：
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作者：
Kalsi KK;Chiesa ST;Trangmar SJ;Ali L;Lotlikar MD;González-Alonso J
这项研究的中心问题是什么？皮肤和肌肉的血流量随着加热而增加，随着降温而减少，但这些反应背后的温度敏感机制尚未完全阐明。主要发现及其重要性是什么？我们发现局部组织充血与红细胞释放的三磷酸腺苷增加有关。增加血管内三磷酸腺苷可增加皮肤和组织的灌注量，使其达到等于或高于热充血的水平。加热和降温改变了分离红细胞的三磷酸腺苷释放。我们的研究结果表明，红细胞通过调节ATP的释放参与血液流动的热调节。局部组织灌注量在加热和降温过程中随着温度的变化而变化，但在热干预过程中用于控制血流的血管ATP信号机制的温度敏感性尚不清楚。在这里，我们测试了这样的假设，即从人的红细胞释放血管扩张介质ATP，而不是从内皮细胞或其他血液成分释放，对温度的升高和降低都很敏感，并且通过ATP输注增加血管内ATP的可用性将加剧肢体组织的热充血。我们首先对健康男性在手臂被动加热和降温过程中的血温、肱动脉血流量和血浆三磷酸腺苷进行了测量，发现它们在受热时分别增加3.0%±1.2C，105.00±0.25mlmin−1和105.00士2.25ml.min−1(均P<0.05)，但随降温而降低或保持不变。在其他男性中，向臂动脉注入三磷酸腺苷可增加皮肤和深层组织的灌注量，使其达到等于或高于热性充血的水平。在暴露于不同温度下的分离的红细胞样品中，三磷酸腺苷的释放从33℃增加到39℃时增加了1.9倍(P<0.05)，在20℃时下降了50%(P<0.05)，但在培养的人内皮细胞、血浆或血清样品中没有观察到变化。总而言之，肢体加热时血浆[ATP]、皮肤和深层组织灌注量的增加与红细胞释放的ATP增加有关，但与内皮细胞或其他血液成分的释放增加无关。红细胞的ATP释放对温度降低也很敏感，这表明在热干预过程中，红细胞可能作为热传感器和ATP信号发生器来控制组织灌注量。
What is the central question of this study? Skin and muscle blood flow increases with heating and decreases with cooling, but the temperature‐sensitive mechanisms underlying these responses are not fully elucidated. What is the main finding and its importance? We found that local tissue hyperaemia was related to elevations in ATP release from erythrocytes. Increasing intravascular ATP augmented skin and tissue perfusion to levels equal or above thermal hyperaemia. ATP release from isolated erythrocytes was altered by heating and cooling. Our findings suggest that erythrocytes are involved in thermal regulation of blood flow via modulation of ATP release. Local tissue perfusion changes with alterations in temperature during heating and cooling, but the thermosensitivity of the vascular ATP signalling mechanisms for control of blood flow during thermal interventions remains unknown. Here, we tested the hypotheses that the release of the vasodilator mediator ATP from human erythrocytes, but not from endothelial cells or other blood constituents, is sensitive to both increases and reductions in temperature and that increasing intravascular ATP availability with ATP infusion would potentiate thermal hyperaemia in limb tissues. We first measured blood temperature, brachial artery blood flow and plasma [ATP] during passive arm heating and cooling in healthy men and found that they increased by 3.0 ± 1.2°C, 105 ± 25 ml min−1 °C−1 and twofold, respectively, (all P < 0.05) with heating, but decreased or remained unchanged with cooling. In additional men, infusion of ATP into the brachial artery increased skin and deep tissue perfusion to levels equal or above thermal hyperaemia. In isolated erythrocyte samples exposed to different temperatures, ATP release increased 1.9‐fold from 33 to 39°C (P < 0.05) and declined by ∼50% at 20°C (P < 0.05), but no changes were observed in cultured human endothelial cells, plasma or serum samples. In conclusion, increases in plasma [ATP] and skin and deep tissue perfusion with limb heating are associated with elevations in ATP release from erythrocytes, but not from endothelial cells or other blood constituents. Erythrocyte ATP release is also sensitive to temperature reductions, suggesting that erythrocytes may function as thermal sensors and ATP signalling generators for control of tissue perfusion during thermal interventions.