Dembowsky K, Czachurski J, Amendt K, Seller H
J Auton Nerv Syst. 1980 Jul;2(2):157-82. doi: 10.1016/0165-1838(80)90043-0.
In chloralose-anaesthetized cats the spinal and supraspinal components of the somato-sympathetic reflex were evoked in the white ramus at T3 and/or L2 by stimulation of intercostal and spinal nerves. A reversible blockade of all ascending and descending spinal pathways was performed by cooling the spinal cord between the second and third cervical segment. Total blockade of conduction was produced at temperatures below 8.5 degrees C (281.5 K). The spinal blockade produced the following reversible effects. (1) Mean arterial pressure fell to 30-50 mm Hg (4.0-6.7 kpa) and the tonic background activity in the white ramus was reduced to 0-24% of control (mean 12.1 +/- 10.0%). (2) The amplitude of the early spinal reflex was increased from 100% to 111-316% (mean 200.9 +/- 49.5%, n = 49) at the thoracic level and to 125-342% (mean 181.4 +/- 74.4%, n = 7) at the lumbar level. The onset latency of the spinal reflex at T3 (range 8-21 msec) was shortened by 0.5-3.0 msec (mean 1.7 +/- 0.9 msec). (3) Supraspinal components were completely abolished. (4) Neither baroreceptor denervation nor midcollicular decerebration altered these effects. (5) The cold block induced increase of the amplitude of the spinal reflex was reduced by the alpha-adrenoceptor agonist clonidine; this effect was reversed by the alpha-adrenoceptor antagonist yohimbine. Selective cooling of the dorsolateral funiculus caused the same effects on the spinal and supraspinal reflexes as cold block of the whole spinal cord. From these findings it is concluded that in the anaesthetized cat the spinal component of the somato-sympathetic reflex is modulated by a descending tonic inhibition. This inhibition acts at both the thoracic and the lumbar level and its origin is in the medulla oblongata. This inhibition is, however, independent of baroreceptor inputs. The pathways descends in the dorsolateral funiculus. It is suggested that noradrenaline or adrenaline might be involved in the transmission of this inhibitory influence.
在水合氯醛麻醉的猫中，通过刺激肋间神经和脊神经，在T3和/或L2的白交通支诱发躯体-交感反射的脊髓和脊髓上成分。通过冷却第二和第三颈椎节段之间的脊髓，对所有上行和下行脊髓通路进行可逆性阻断。在温度低于8.5℃（281.5K）时产生完全的传导阻断。脊髓阻断产生了以下可逆性效应。（1）平均动脉压降至30 - 50mmHg（4.0 - 6.7kPa），白交通支的紧张性背景活动降至对照的0 - 24%（平均12.1±10.0%）。（2）在胸段，早期脊髓反射的幅度从100%增加到111 - 316%（平均为200.9±49.5%，n = 49），在腰段增加到125 - 342%（平均为181.4±74.4%，n = 7）。T3处脊髓反射的起始潜伏期（范围8 - 21毫秒）缩短了0.5 - 3.0毫秒（平均1.7±0.9毫秒）。（3）脊髓上成分完全消失。（4）压力感受器去神经支配和中脑桥脑断离均未改变这些效应。（5）α-肾上腺素能激动剂可乐定可降低冷阻断引起的脊髓反射幅度增加；α-肾上腺素能拮抗剂育亨宾可逆转此效应。背外侧索的选择性冷却对脊髓和脊髓上反射产生的效应与整个脊髓的冷阻断相同。从这些发现可以得出结论，在麻醉猫中，躯体-交感反射的脊髓成分受下行紧张性抑制的调节。这种抑制作用于胸段和腰段，其起源于延髓。然而，这种抑制与压力感受器输入无关。该通路在背外侧索下行。提示去甲肾上腺素或肾上腺素可能参与这种抑制性影响的传递。
