选择性阳离子在网膜内神经脱敏中的作用。

K Markowitz, S Kim
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引用次数: 0

摘要

牙本质敏感是病人的常见主诉。牙骨质或牙釉质的移除会暴露牙本质,使各种刺激通过牙本质小管产生液体运动。这些液体的运动被认为会激活牙髓感觉神经,导致疼痛。已经研究了各种治疗方法来治疗这个问题。树脂、氟化物和草酸盐溶液被用来堵塞牙本质小管。KNO3和SrCl2是脱敏牙膏的活性成分,但两者都不能降低牙本质的通透性。研究了不同溶液对麻醉猫犬齿高渗(3M NaCl)引起的神经活动的抑制作用。兴奋和脱敏的溶液被放置在一个深牙本质腔准备在切牙髓角。一个用来记录神经活动的电极也被放置在这个深腔中。KNO3和其他含K+离子的溶液对神经活动产生双相效应。在将这些溶液应用于牙本质深部腔后,立即出现短暂的高频尖峰活动。在短暂的兴奋期之后,网膜内神经沉默,对高渗NaCl的反应较弱。CaCl2和其他二价阳离子溶液也能抑制高渗NaCl诱导的神经活动,但作用弱于K+。这些观察结果可以根据不同离子对神经兴奋性的影响来解释。增加牙本质神经末梢附近的钾离子浓度,使其去极化并激活神经纤维。经过长时间的去极化后,动作电位机制失效。二价阳离子溶液稳定神经膜而不改变膜电位。脱敏溶液不会通过影响髓血流量而降低神经活动。这个实验模型并不能完全解释这些脱敏剂的临床作用。目前正在研究炎症在过敏和牙痛中的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The role of selected cations in the desensitization of intradental nerves.

Dentinal sensitivity is a common complaint of patients. Removal of cementum or enamel leaves the dentin exposed allowing various stimuli to produce fluid movement through the dentinal tubules. These fluid movements are believed to activate pulpal sensory nerves leading to pain. Various therapeutic approaches have been investigated to treat this problem. Resins, fluoride compounds and oxalate solutions have been used to block the dentinal tubules. KNO3 and SrCl2 are active ingredients in desensitizing tooth pastes but neither compound reduces the permeability of dentine. The ability of various solutions to decrease hypertonic (3M NaCl) evoked nerve activity was tested in the canine teeth of anesthetized cats. Excitatory and desensitizing solutions were placed into a deep dentinal cavity prepared over the incisal pulp horn. An electrode used to record nerve activity was also placed into this deep cavity. KNO3 and other K+ ion containing solutions elicit a biphasic effect on nerve activity. Immediately following application of these solutions into the deep dentinal cavity there is a brief burst of high frequency spike activity. Following this brief period of excitation, the intradental nerves are silent and respond weakly to hypertonic NaCl. CaCl2 and other divalent cation solutions also inhibit hypertonic NaCl induced nerve activity, but have a weaker effect than that exerted by K+. These observations can be explained based on the effects of various ions on nerve excitability. Increasing the K+ ion concentration in the vicinity of the dentinal nerve terminal depolarize and activates the nerve fibers. Following a prolonged period of depolarization the action potential mechanism is inactivated. Divalent cation solutions stabilize the nerve membrane without changing the membrane potential. Desensitizing solutions do not decrease nerve activity by an effect on pulpal blood flow. This experimental model does not entirely explain the clinical action of these desensitizing agents. The role of inflammation in hypersensitivity and dental pain is currently being investigated.

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