Garrett J R
J Dent Res. 1987 Feb;66(2):387-97. doi: 10.1177/00220345870660020201.
Consideration of the history of this subject has created a perspective which helps one to appreciate how errors in thinking have occurred and why some have persisted, despite subsequent improvements in information. The most enduring misconception has been that the drying of the mouth under stress is due to sympathetic inhibitory fibers, a view that must be eradicated, for such fibers do not exist. The inhibition is due to central influences from higher centers acting on the salivary centers and thereby suppressing reflex activity. Wide variations exist in the neuro-effector arrangements and in the cellular responses in different glands from different species. Myoepithelial cells are usually contracted by both parasympathetic and sympathetic nerves. The blood vessels also receive a dual innervation, but parasympathetic impulses cause vasodilatation as part of secretion, whereas the sympathetic vasoconstrictor fibers are part of a more generalized vascular control system and not a direct part of the reflex secretory sympathetic pathway. Parasympathetic drive usually provides the main stimulus for fluid formation by parenchymal cells, whereas sympathetic nerves tend to increase the output of pre-formed components from certain cells. Absence of nerve impulses causes variable atrophic and other metabolic effects on the parenchymal cells. Evidence is beginning to accrue that certain nerve impulses may influence resynthetic activities. Vacuolation, often found experimentally after strong stimulation, also occurs to a variable extent in certain cells as a normal part of reflex secretion and may therefore have an effect on the components entering the saliva. If rupture of vacuoles occurs, then this may contribute to the salivary amylase that is present in the blood. Recent evidence points to the possibility that, even in a monomorphic gland, not all of the components necessarily enter nerve-induced saliva in "parallel" proportions. Consideration of current information has enabled some provisional generalizations about the roles of the secretory nerves to be suggested in the summary, but they must not be considered immutable.
对该主题历史的思考形成了一种视角,有助于人们理解思维错误是如何发生的,以及为什么有些错误尽管后来信息有所改进却依然存在。最持久的误解是,压力下口腔干燥是由于交感抑制纤维所致,这种观点必须根除,因为这种纤维并不存在。抑制是由于高级中枢对唾液中枢的中枢性影响,从而抑制反射活动。不同物种不同腺体的神经效应器排列和细胞反应存在广泛差异。肌上皮细胞通常由副交感神经和交感神经共同收缩。血管也接受双重神经支配,但副交感神经冲动在分泌过程中会引起血管舒张,而交感缩血管纤维是更广泛的血管控制系统的一部分,并非反射性分泌交感神经通路的直接组成部分。副交感神经驱动通常为实质细胞形成液体提供主要刺激,而交感神经倾向于增加某些细胞中预先形成成分的输出。神经冲动的缺失会对实质细胞产生不同程度的萎缩和其他代谢影响。越来越多的证据表明,某些神经冲动可能会影响再合成活动。空泡化现象在实验中常于强烈刺激后出现,在某些细胞中作为反射性分泌的正常组成部分也会不同程度地发生,因此可能会对进入唾液的成分产生影响。如果空泡破裂,那么这可能会导致血液中出现唾液淀粉酶。最近的证据表明,即使在单形性腺中,并非所有成分都必然以“平行”比例进入神经诱导的唾液中。对当前信息的思考使得在总结中能够提出一些关于分泌神经作用的初步概括,但这些概括不应被视为一成不变的。