Marshall J M
J Auton Nerv Syst. 1981 Apr;3(2-4):389-400. doi: 10.1016/0165-1838(81)90077-1.
It has been shown recently that in the cat anesthetized with althesin, stimulation of carotid chemoreceptors evokes the autonomic components of the alerting stage of the defence reaction including cholinergic vasodilatation in skeletal muscle. The discrepancy between this result and those of previous experiments on animals anethetized with chloralose or barbiturates may be reconciled when it is realized that these more conventional anesthetics prevent normal transmission through the defence areas. The obvious conclusion, that activation of the defence area is an integral part of the response to peripheral chemoreceptor stimulation indicates that the question of interaction between baro- and chemoreceptor responses should be reconsidered, particularly as it is known that the baroreceptor reflex is suppressed when the defence areas are activated by central stimulation. The present paper describes experiments performed on Althesin-anesthetized cats in which carotid baroreceptors were stimulated by inflating a blind sac and carotid chemoreceptors were stimulated by injections of inorganic phosphate solution or saline equilibrated with CO2. The results showed that the baroreceptor reflex may be fully suppressed when the autonomic components of the alerting response were evoked by chemoreceptor stimulation. In some cases however, when the activation of the defence areas was mild, at least as judged by the magnitude of the cholinergic vasodilatation evoked by the chemoreceptor stimulus alone, there appeared to be algebraic summation of the baro- and chemoreceptor response. It is concluded that the extent to which a given chemoreceptor stimulus suppresses the baroreceptor reflex is dependent on its potency as a stimulus to the defence areas. It is suggested that the chemoreceptor input may be more important than hitherto suspected in setting the level of arterial blood pressure.
最近研究表明,在使用安泰酮麻醉的猫身上,刺激颈动脉化学感受器会引发防御反应警觉阶段的自主神经成分,包括骨骼肌中的胆碱能血管舒张。当认识到这些更传统的麻醉剂会阻止通过防御区域的正常传导时,这一结果与之前用氯醛糖或巴比妥类药物麻醉动物的实验结果之间的差异就可以得到解释。明显的结论是,防御区域的激活是对外周化学感受器刺激反应的一个组成部分,这表明压力感受器和化学感受器反应之间的相互作用问题应该重新考虑,特别是因为已知当防御区域被中枢刺激激活时,压力感受器反射会受到抑制。本文描述了在使用安泰酮麻醉的猫身上进行的实验,其中通过向一个盲囊充气来刺激颈动脉压力感受器,通过注射无机磷酸盐溶液或用二氧化碳平衡的盐水来刺激颈动脉化学感受器。结果表明,当化学感受器刺激引发警觉反应的自主神经成分时,压力感受器反射可能会被完全抑制。然而,在某些情况下,当防御区域的激活较轻时,至少从仅由化学感受器刺激引发的胆碱能血管舒张的程度来判断,压力感受器和化学感受器反应似乎存在代数相加。得出的结论是,给定的化学感受器刺激抑制压力感受器反射的程度取决于其作为对防御区域刺激的效力。有人提出,化学感受器输入在设定动脉血压水平方面可能比迄今为止所怀疑的更为重要。