Conradt M, Kullmann R, Matsuzaki T, Simon E
Basic Res Cardiol. 1975 Jan-Feb;70(1):10-28. doi: 10.1007/BF01905550.
Dogs were anesthetized with sodium pentobarbital, relaxed with succinyl choline and were kept under artificial ventilation. Both carotid bifurcations were denervated and the Vagus nerves were cut in the neck. Regional blood flow in the skin and the intestine, cardiac output, heart rate and arterial pressure were determined before, during and after spinal cord heating and cooling. Further experiments were performed in which, in addition, sympathetic effects on the heart were excluded by exstirpation of the caudal cervical and stellate ganglia or by beta-receptor blockade. The cardiovascular responses were compared with those obtained in a preceding investigation from dogs with intact baroreceptors and vagus nerves. As in intact dogs, appropiate thermoregulatory adjustments of skin blood flow were induced by thermal stimulation of the spinal cord after baroreceptor denervation and vagotomy. However, blood pressure homeostasis was lost. The pattern of cardiovascular ajustments during heating consisted in cutaneous vasodilatation intestinal vasoconstriction and, due to sympathetic activation an increase of heart rate and cardiac output. This pattern was qualitatively identical with that intact animals. During spinal cord cooling the cardiovascular response pattern consisted in cutaneous vasoconstriction, intestinal vasoconstriction and, depending on cooling intensity, a reduced or unchanged sympathetic influence on the heart. This pattern differed considerably from what in intact animals but basic features were still present as indicated by opposite changes of cardiac and vascular sympathetic tone during cooling. It is concluded that the baroreceptor signals play no primary role in the generation of differential vasomotor responses under the present experimental conditions. This confirms assumptions made on the basis of observations in animals with intact baroreceptor input. However, baroreceptor signals contribute significantly to blood pressure homeostasis which is normally maintained during spinal thermal stimulation.
用戊巴比妥钠对狗进行麻醉，用琥珀酰胆碱使其松弛，并维持人工通气。双侧颈动脉分叉处去神经支配，迷走神经在颈部切断。在脊髓加热和冷却前、期间和之后，测定皮肤和肠道的局部血流量、心输出量、心率和动脉血压。还进行了进一步的实验，另外通过切除颈尾神经节和星状神经节或通过β受体阻断来排除交感神经对心脏的影响。将心血管反应与先前对具有完整压力感受器和迷走神经的狗进行的研究中获得的反应进行比较。与完整的狗一样，在压力感受器去神经支配和迷走神经切断后，脊髓的热刺激诱导了皮肤血流量的适当体温调节调整。然而，血压稳态丧失。加热期间的心血管调整模式包括皮肤血管舒张、肠道血管收缩，并且由于交感神经激活，心率和心输出量增加。这种模式在质量上与完整动物的模式相同。在脊髓冷却期间，心血管反应模式包括皮肤血管收缩、肠道血管收缩，并且根据冷却强度，交感神经对心脏的影响降低或不变。这种模式与完整动物的模式有很大不同，但基本特征仍然存在，如冷却期间心脏和血管交感神经张力的相反变化所示。得出的结论是，在目前的实验条件下，压力感受器信号在差异性血管运动反应的产生中不发挥主要作用。这证实了基于对具有完整压力感受器输入的动物的观察所做出的假设。然而，压力感受器信号对血压稳态有显著贡献，血压稳态在脊髓热刺激期间通常得以维持。
