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一氧化氮介导辣椒素引起的耳蜗血流量增加。

Nitric oxide mediates capsaicin-induced increase in cochlear blood flow.

作者信息

Vass Z, Brechtelsbauer P B, Nuttall A L, Miller J M

机构信息

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

出版信息

Hear Res. 1996 Oct;100(1-2):114-9. doi: 10.1016/0378-5955(96)00102-5.

DOI:10.1016/0378-5955(96)00102-5
PMID:8922985
Abstract

Capsaicin has been previously shown to increase cochlear blood flow (CBF) in a dose-dependent manner. The aim of this study was to define the role of nitric oxide (NO) in capsaicin-induced changes in CBF. This was investigated in the anesthetized guinea pig, utilizing laser Doppler flowmetry. Application of capsaicin (64.8 and 6.48 nmol in 2 microliters of saline) to the round window membrane (RWM) caused increases in CBF (34 +/- 2.8% of baseline (BL) and 28 +/- 2.3% BL, respectively (P < 0.001)). Application of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg intravenously or topically to the RWM) reduced blood flow in the cochlea, as previously reported. After pretreatment with i.v. L-NAME, the effect of capsaicin on CBF was significantly decreased. With the dose of capsaicin at 64.8 nmol, the increase in CBF fell from 34 +/- 2.8% BL to 6.9 +/- 1.5% BL (P < 0.001), and at 6.48 nmol it fell from 28 +/- 2.3% BL to 4.8 +/- 1.6% BL (P < 0.001). RWM L-NAME application also decreased the capsaicin vasodilatation effect. A capsaicin dose of 64.8 nmol resulted in only a 10 +/- 2.5% BL increase in CBF, and with 6.48 nmol capsaicin the increase was 7.8 +/- 2.2% of BL (P < 0.001). Capsaicin-sensitive sensory neurons in other systems are generally known to release substance P (SP), which in turn elicits release of endothelium derived relaxing factor (NO). The results of this study indicate that NO is a mediator of capsaicin-sensitive sensory neuronal function in CBF regulation.

摘要

辣椒素此前已被证明能以剂量依赖的方式增加耳蜗血流量(CBF)。本研究的目的是确定一氧化氮(NO)在辣椒素诱导的CBF变化中的作用。在麻醉的豚鼠身上利用激光多普勒血流仪对此进行了研究。将辣椒素(64.8和6.48纳摩尔溶于2微升盐水中)应用于圆窗膜(RWM)会导致CBF增加(分别为基线(BL)的34±2.8%和28±2.3%,P<0.001)。如先前报道,应用NO合酶抑制剂NG-硝基-L-精氨酸甲酯(L-NAME)(静脉注射10毫克/千克或局部应用于RWM)会降低耳蜗中的血流量。静脉注射L-NAME预处理后,辣椒素对CBF的作用显著降低。当辣椒素剂量为64.8纳摩尔时,CBF的增加从34±2.8% BL降至6.9±1.5% BL(P<0.001),当剂量为6.48纳摩尔时,从28±2.3% BL降至4.8±1.6% BL(P<0.001)。局部应用于RWM的L-NAME也降低了辣椒素的血管舒张作用。64.8纳摩尔的辣椒素剂量仅导致CBF增加10±2.5% BL,6.48纳摩尔的辣椒素剂量导致的增加为BL的7.8±2.2%(P<0.001)。其他系统中对辣椒素敏感的感觉神经元通常已知会释放P物质(SP),而P物质又会引发内皮衍生舒张因子(NO)的释放。本研究结果表明,NO是CBF调节中对辣椒素敏感的感觉神经元功能的介质。

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