The effect of arterial occlusion on sweat‐gland responses in the human forearm
The effect of arterial occlusion on sweat‐gland responses in the human forearm
复制标题
动脉闭塞对人体前臂汗腺反应的影响
DOI：
10.1113/jphysiol.1959.sp006310
复制
发表时间：
1959
期刊：
影响因子：
--
通讯作者：
J. Weiner
中科院分区：
文献类型：
--
作者：
K. Collins;F. Sargent;J. Weiner
众所周知，出汗肢体的血液供应受阻会导致出汗量减少（van Heyningen & Weiner，1952；Kuno，1956）和活跃腺体数量减少（Randall，Deering & Dougherty，1948）。汗液的成分也会发生变化（Ladell，1951；van Heyningen & Weiner，1952）。 30 分钟后释放闭塞后，输出和成分都会恢复。 Randall 等人认为，在动脉闭塞期间，汗腺会对强烈的辐射热做出反应。 (1948) 认为缺血性抑制主要是对神经末梢和可能的催汗神经轴突的影响，而不是腺细胞本身的衰竭。然而，阿托品化或去神经化的腺体均已被证明对乙酰胆碱不敏感，也对辐射热的直接刺激有反应（Randall，1947；Janowitz & Grossmann，1950）。兰德尔等人的证据。因此，（1948）并不排除另一种选择，即在缺血期间神经仍然能够产生递质，但腺细胞对递质的反应减弱。 Sonnenschein、Kobrin、Janowitz 和 Grossman (1951) 的论文支持了这一替代假设，他们对动脉闭塞期间汗腺对乙酰胆碱反应的减弱进行了简要评论。鉴于这些相互矛盾的理论，进行了实验，试图阐明出汗机制失效的性质和部位。关于这些研究结果的初步报告之前已发布（Collins、Sargent & Weiner，1958）。
It is well known that obstruction of the blood supply to a sweating limb results in a diminution in the output of sweat (van Heyningen & Weiner, 1952; Kuno, 1956) and a decline in the number of active glands (Randall, Deering & Dougherty, 1948). Changes also occur in the composition of sweat (Ladell, 1951; van Heyningen & Weiner, 1952). There is recovery of both output and composition when the occlusion is released after 30 min. The fact that the sweat glands respond to intense radiant heat during arterial occlusion suggested to Randall et al. (1948) that the ischaemic depression was primarily an effect on the nerve endings and possibly axons of the sudomotor nerves and not a failure of the gland cells themselves. However, atropinized or denervated glands, both of which have been shown to be insensitive to acetylcholine, also respond to direct stimulation by radiant heat (Randall, 1947; Janowitz & Grossmann, 1950). The evidence of Randall et al. (1948) does not therefore preclude the alternative that during ischaemia the nerve is still capable of producing transmitter but that the response of the gland cells to the transmitter is reduced. Support for this alternative hypothesis appears in the paper by Sonnenschein, Kobrin, Janowitz & Grossman (1951) who comment briefly on a diminution of the sweat-gland response to acetylcholine during arterial occlusion. In view of these conflicting theories experiments were undertaken in an attempt to clarify the nature and site of the failure of the sweating mechanism. A preliminary report on the results of these studies has previously been communicated (Collins, Sargent & Weiner, 1958).