Fagius J, Karhuvaara S, Sundlöf G
Department of Neurology, University Hospital, Uppsala, Sweden.
Acta Physiol Scand. 1989 Nov;137(3):325-34. doi: 10.1111/j.1748-1716.1989.tb08760.x.
Micro-electrode multi-unit recordings of muscle nerve sympathetic activity (MSA) involved in cardiovascular homeostasis or skin nerve sympathetic activity (SSA) involved in thermoregulation were made in the right peroneal nerve of 48 healthy volunteers during performance of the cold pressor test, i.e. immersion of one hand in ice water (2 +/- 0.5 degrees C) for 1 min. Eleven subjects underwent the same procedure on a second MSA recording occasion. As a rule, immersion evoked an increase in MSA, with a gradual decrease on emersion. The response showed a wide range of variation between and within subjects; the intra-individual difference between first and second immersion on the same recording occasion was up to sevenfold, and from first to second recording up to fivefold. The increase in MSA correlated with the degree of discomfort from the ice water. In nine subjects with a large increase in MSA on ice water immersion, intracutaneous painful electrical stimulation to a level equalling the discomfort from the ice water was added, but it was not accompanied by any change in MSA. The increase in MSA was accompanied by and correlated quite well with an increase in blood pressure. Intra-arterial blood pressure recordings showed that MSA occurred at pressure levels normally associated with total inhibition of MSA, and that an inverse linear relationship between diastolic blood pressure and MSA at rest was abolished during the ice water immersion. SSA showed no consistent change with ice water immersion. It is concluded that the cold pressor test is a powerful activator of MSA, i.e. baroreceptor-governed vasoconstrictor outflow; that MSA contributes to the blood pressure elevation with this manoeuvre; that MSA operates at another blood pressure level during the manoeuvre and that the baroreflex inhibitory level consequently is changed; and that the response is not a reaction to pain only.
在48名健康志愿者进行冷加压试验（即将一只手浸入2±0.5摄氏度的冰水中1分钟）期间，对参与心血管稳态调节的肌肉神经交感神经活动（MSA）或参与体温调节的皮肤神经交感神经活动（SSA）进行了微电极多单位记录，记录部位为右侧腓总神经。11名受试者在第二次进行MSA记录时重复了相同的操作。通常情况下，浸入冰水会引起MSA增加，出水时逐渐下降。该反应在受试者之间和受试者内部存在很大差异；在同一记录时段，第一次和第二次浸入之间的个体内差异高达7倍，从第一次记录到第二次记录差异高达5倍。MSA的增加与冰水引起的不适程度相关。在9名冰水浸入时MSA大幅增加的受试者中，增加了皮内疼痛性电刺激，使其达到与冰水不适程度相当的水平，但这并未伴随MSA的任何变化。MSA的增加伴随着血压升高，且二者相关性良好。动脉内血压记录显示，MSA发生在通常与MSA完全抑制相关的压力水平，并且在冰水浸入期间，静息时舒张压与MSA之间的反向线性关系消失。SSA在冰水浸入时没有一致的变化。结论是，冷加压试验是MSA（即压力感受器控制的血管收缩传出神经活动）的强力激活剂；通过该操作，MSA有助于血压升高；在该操作期间，MSA在另一个血压水平起作用，因此压力反射抑制水平发生改变；并且该反应不仅仅是对疼痛的反应。
