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首页> 外文期刊>Journal of Pharmacological and Toxicological Methods >Neurophysiological assessment of sympathetic cardiovascular activity after loss of postganglionic neurons in the anesthetized rat
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Neurophysiological assessment of sympathetic cardiovascular activity after loss of postganglionic neurons in the anesthetized rat

机译：麻醉大鼠猝灭神经元损失后交感神经心血管活性的神经生理学评估

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The goal of this study was to determine the degree of sympathetic postganglionic neuronal loss required to impair cardiovascular-related sympathetic activity. To produce neuronal loss separate groups of rats were treated daily with guanethidine for either 5 days or 11 days, followed by a recovery period. Sympathetic activity was measured by renal sympathetic nerve activity (RSNA). Stereology of thoracic (T13) ganglia was performed to determine neuronal loss. Despite loss of more than two thirds of neurons in T13 ganglia in both treated groups no effect on resting blood pressure (BP) or heart rate (HR) was detected. Basal RSNA in rats treated for 5 days (0.61 +/- 0.10 mu V * s) and 11 days (0.37 +/- 0.08 mu V * s) was significantly less than vehicle-treated rats (0.99 +/- 0.13 mu V * s, p < 0.05). Increases in RSNA by baroreceptor unloading were significantly lower in 5-day (1.09 +/- 0.19 mu V * s) and 11-day treated rats (0.59 +/- 0.11 mu V * s) compared with vehicle-treated rats (1.82 +/- 0.19 mu V * s, p < 0.05). Increases in RSNA to chemoreceptor stimulation were significantly lower in 5-day treated rats (1.54 +/- 0.25 mu V * s) compared with vehicle-treated rats (2.69 +/- 0.23 mu V * s, p < 0.05). Increases in RSNA in 11-day treated rats were significantly lower (0.75 +/- 0.15 mu V * s, p < 0.05) compared with both vehicle-treated and 5-day treated rats. A positive correlation of neurons to sympathetic responsiveness but not basal activity was detected. These data suggest that diminished capacity for reflex sympathetic responsiveness rather than basal activity alone must be assessed for complete detection of neurophysiological cardiovascular impairment. (C) 2016 Elsevier Inc. All rights reserved.
机译：本研究的目标是确定损害心血管相关的交感神经活动所需的交感神经损失程度。为了产生神经元损失，将单独的大鼠组每天用胍丝氨酸治疗5天或11天，然后进行恢复期。通过肾交感神经活性（RSNA）测量交感神经活性。进行胸部（T13）神经节的立体学，以确定神经元损失。尽管在两种治疗组的T13神经节中丧失了超过三分之二的神经元，但没有对检测到静息血压（BP）或心率（HR）的影响。治疗5天（0.61 +/-0.10μm）和11天（0.37 +/-0.08μmV* s）的大鼠的基础rsna显着低于载体处理的大鼠（0.99 +/-0.13μmV* s，p <0.05）。在5天（1.09 +/-0.19μmV* s）和11天处理的大鼠（0.59 +/-0.11μmv* s）与载体处理的大鼠相比/ - 0.19 mu v * s，p <0.05）。与载体处理的大鼠相比，5天处理大鼠（1.54 +/-0.25μm）的5天处理大鼠（1.54 +/-0.25μm）显着降低了Chemereptover刺激的增加（2.69 +/-0.23μmV* s，p <0.05）。与载体处理和5天处理过5天的大鼠相比，11天治疗大鼠中RSNA中的RSNA增加显着降低（0.75 +/-0.15μm，P <0.05）。检测神经元对交感感应性但不是基底活性的正相关性。这些数据表明，必须评估反射交感神经响应性的能力，而不是基于基础活性，以完全检测神经生理心血管损伤。 （c）2016年Elsevier Inc.保留所有权利。

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