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电刺激引起的耳蜗血流量增加:I. 频率和强度效应。

Electrically stimulated increases in cochlear blood flow: I. Frequency and intensity effects.

作者信息

Sillman J S, LaRouere M J, Masta R I, Miller J M, Nuttall A L

机构信息

Kresge Hearing Research Institute, University of Michigan, Ann Arbor 48109-0506.

出版信息

Otolaryngol Head Neck Surg. 1989 Apr;100(4):308-16. doi: 10.1177/019459988910000411.

Abstract

Charge-balanced, sinusoidal current was passed differentially between the apex and round window of the guinea pig cochlea. Cochlear blood flow was measured using a laser Doppler flow monitor. Systemic blood pressure was monitored from a cannula within the common carotid artery. Electrical stimulation increased cochlear blood flow, while systemic blood pressure was unaffected. A cochlear blood flow response parameter, normalized for transient changes in systemic blood pressure, was defined. The magnitude of the response parameter was found to be frequency selective and was also found to be an increasing function of current intensity, with maximum responses obtained with 500 Hz sinusoids. This cochlear blood flow response was not observed in dead animals; was present in preparations paralyzed with gallamine hydrochloride; and was correlated with an increase in cochlear red blood cell velocity, as directly observed by intravital microscopy. These observations imply that electrical stimulation induces a local vasodilation within the temporal bone. The fact that decreased cochlear blood flow was never observed with current injection implies that ischemia is not a likely mechanism of electrically induced tissue damage within the inner ear. The mechanism of this cochlear blood flow response is addressed in a companion report.

摘要

电荷平衡的正弦电流在豚鼠耳蜗的顶点和圆窗之间进行差分传递。使用激光多普勒血流监测仪测量耳蜗血流量。通过颈总动脉内的插管监测全身血压。电刺激增加了耳蜗血流量,而全身血压未受影响。定义了一个针对全身血压瞬态变化进行归一化的耳蜗血流量反应参数。发现反应参数的大小具有频率选择性,并且也是电流强度的递增函数,在500 Hz正弦波时获得最大反应。在死亡动物中未观察到这种耳蜗血流量反应;在被盐酸加拉明麻痹的制剂中存在;并且与耳蜗红细胞速度的增加相关,这是通过活体显微镜直接观察到的。这些观察结果表明电刺激会在颞骨内诱导局部血管舒张。电流注入从未观察到耳蜗血流量减少这一事实表明,缺血不太可能是内耳电诱导组织损伤的机制。这份配套报告探讨了这种耳蜗血流量反应的机制。

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