Dept. of Physiology, Univ. of Texas Health Science Center, 7703 Floyd Curl Dr., San Antonio TX 78231, USA.
J Appl Physiol (1985). 2010 Oct;109(4):1229-38. doi: 10.1152/japplphysiol.00407.2010. Epub 2010 Jun 3.
The level of skin blood flow is subject to both reflex thermoregulatory control and influences from the direct effects of warming and cooling the skin. The effects of local changes in temperature are capable of maximally vasoconstricting or vasodilating the skin. They are brought about by a combination of mechanisms involving endothelial, adrenergic, and sensory systems. Local warming initiates a transient vasodilation through an axon reflex, succeeded by a plateau phase due largely to nitric oxide. Both phases are supported by sympathetic transmitters. The plateau phase is followed by the die-away phenomenon, a slow reversal of the vasodilation that is dependent on intact sympathetic vasoconstrictor nerves. The vasoconstriction with local skin cooling is brought about, in part, by a postsynaptic upregulation of α(2c)-adrenoceptors and, in part, by inhibition of the nitric oxide system at at least two points. There is also an early vasodilator response to local cooling, dependent on the rate of cooling. The mechanism for that transient vasodilation is not known, but it is inhibited by intact sympathetic vasoconstrictor nerve function and by intact sensory nerve function.
皮肤血流量既受到反射性体温调节控制,也受到皮肤加热和冷却直接影响的影响。局部温度变化的影响能够使皮肤最大程度地收缩或扩张血管。这些影响是由涉及内皮细胞、肾上腺素能和感觉系统的多种机制共同作用产生的。局部加热通过轴突反射引发短暂的血管扩张,随后由于一氧化氮的作用进入平台期。这两个阶段都得到交感神经递质的支持。平台期之后是消退现象,即血管扩张的缓慢逆转,这依赖于完整的交感神经血管收缩神经。局部皮肤冷却引起的血管收缩部分是由于突触后α(2c)-肾上腺素能受体的上调,部分是由于至少两个部位的一氧化氮系统的抑制。局部冷却还会引起早期的血管扩张反应,这取决于冷却的速度。这种短暂血管扩张的机制尚不清楚,但它受到完整的交感神经血管收缩神经功能和完整的感觉神经功能的抑制。