Skin sympathetic nerve activity component synchronizing with cardiac cycle is involved in hypovolaemic suppression of cutaneous vasodilatation in hyperthermia
Skin sympathetic nerve activity component synchronizing with cardiac cycle is involved in hypovolaemic suppression of cutaneous vasodilatation in hyperthermia
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DOI：
10.1113/jphysiol.2011.220251
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发表时间：
2011-12-01
影响因子：
5.5
通讯作者：
Nose, Hiroshi
中科院分区：
文献类型：
--
作者：
Kamijo, Yoshi-ichiro;Okada, Yoshiyuki;Nose, Hiroshi
尽管体温过高的皮肤血管扩张在低血容量时受到抑制，但介导这种抑制的传出神经通路尚未确定。为了确定抑制低血容量时皮肤血管扩张的神经电信号，对20名健康受试者在正常血容量(n=10)和低血容量(n=10)条件下，在被动升温45min前和45min期间测量了同侧足背激光多普勒血流量(LDF)、平均动脉压(MAP)和食道温度(T-OES)，并进行了腓神经皮肤交感神经电活动(SSNA)和显微神经学检查。低血容量是通过给药利尿剂来实现的。在升温结束时，两组的皮肤血管电导(CVC=LDF/MAP)、SSNA突发频率和从整流和滤波的SSNA信号中获得的总SSNA随着T-OES的增加而增加，接近0.5℃。低血容量组中心静脉容量的增加明显低于正常血容量组(P<；0.0001)，而猝发频率和总SSNA的增加在两组间无显著差异(P>；0.32)。然而，使用另一种分析方法，即在给定R波之后的5个S期间，使用0.05%的S频段从原始信号构建棘波发生直方图，我们发现SSNA分量与心动周期同步，S潜伏期为1.1-1.3。这种成分随着T-OES的增加而增加，并且这种增加被低血容量显著抑制(P<；0.0001)。综上所述，高温期间皮肤血管扩张的低血容量性抑制可能是由于与心脏周期同步的SSNA成分减少所致。
Although cutaneous vasodilatation in hyperthermia was suppressed during hypovolaemia, the efferent neural pathway mediating this suppression has not been identified. To determine the electrical nerve signals which account for the suppression of cutaneous vasodilatation during hypovolaemia, skin sympathetic nerve activity (SSNA; microneurography) from the peroneal nerve, laser-Doppler blood flow (LDF) on the ipsilateral dorsal foot, mean arterial pressure (MAP; sonometry) and oesophageal temperature (T-oes) were measured before and during 45 min of passive warming in 20 healthy subjects during normovolaemia (n = 10) or hypovolaemia (n = 10) conditions. Hypovolaemia was achieved by diuretic administration. Cutaneous vascular conductance (CVC = LDF/MAP), SSNA burst frequency and total SSNA obtained from rectified and filtered SSNA signal increased as T-oes increased by similar to 0.5 degrees C by the end of warming in both groups. The increase in CVC was significantly lower in hypovolaemia than normovolaemia (P < 0.0001), but with no significant difference in the increase in burst frequency and total SSNA between groups (P > 0.32). However, using an alternative analysis that constructed spike incidence histograms from the original signal using 0.05 s bins during the 5 s following a given R-wave, we found a SSNA component synchronized with the cardiac cycle with a 1.1-1.3 s latency. This component increased with an increase in T-oes and the increase was significantly suppressed by hypovolaemia (P < 0.0001). In conclusion, hypovolaemic suppression of cutaneous vasodilatation during hyperthermia might be caused by a reduction in the SSNA component synchronized with cardiac cycle.