• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Cardiovascular regulation after destruction of the C1 cell group of the rostral ventrolateral medulla in rats.
【24h】

Cardiovascular regulation after destruction of the C1 cell group of the rostral ventrolateral medulla in rats.

机译：破坏大鼠头侧腹外侧延髓的C1细胞群后的心血管调节。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

To evaluate the role of C1 neurons in the rostral ventrolateral medulla (RVLM) in cardiovascular regulation, we studied rats in which this cell group was destroyed by the injection of anti-dopamine-beta-hydroxylase-saporin into the RVLM. These immunotoxin injections resulted in 32-99% depletion of the RVLM-C1 neurons and approximately 50% depletion of the A5 cell population. In conscious rats with large (>80%) depletion of the RVLM-C1 cell population, resting arterial pressure was approximately 10 mmHg lower than in control injected rats, although heart rate was not significantly different. Similar results were observed when arterial pressure was recorded in urethan-anesthetized rats, although under anesthesia, heart rate was also reduced in rats with large (>80%) depletion of the RVLM-C1 neuronal population. Sympathoexcitatory responses to baroreceptor unloading, chemoreceptor activation, and electrical stimulation of sciatic nerve afferent fibers were attenuated in rats with >80% depletion of the RVLM-C1 cell population. These effects of RVLM-C1 plus A5 cell populations were not mimicked by either smaller lesions of the RVLM-C1 population or by selective destruction of the A5 cell population with 6-hydroxydopamine. Sympathoinhibitory responses such as decreases in arterial pressure and heart rate evoked by injection of GABA into the RVLM or by intravenous phenylbiguanide administration were not altered by RVLM-C1 plus A5 cell depletion. These data suggest that RVLM-C1 cells contribute to the maintenance of baseline arterial pressure and play an integral role in sympathoexcitatory responses.
机译：为了评估C1神经元在延髓腹侧延髓（RVLM）的心血管调节中的作用，我们研究了通过向RVLM中注射抗多巴胺-β-羟化酶-saporin破坏该细胞群的大鼠。这些免疫毒素注射导致RVLM-C1神经元消耗32-99％，A5细胞群消耗约50％。在有大量（> 80％）RVLM-C1细胞耗竭的清醒大鼠中，静息动脉压比对照注射大鼠低约10 mmHg，尽管心率无显着差异。当在经尿烷麻醉的大鼠中记录到动脉压时，观察到了相似的结果，尽管在麻醉下，RVLM-C1神经元细胞大量耗竭的大鼠的心率也降低了。在RVLM-C1细胞耗竭> 80％的大鼠中，对压力感受器卸载，化学感受器激活和坐骨神经传入纤维电刺激的交感兴奋反应减弱。 RVLM-C1群体的较小病变或用6-羟基多巴胺选择性破坏A5细胞群体均不能模仿RVLM-C1和A5细胞群体的这些作用。 RVLM-C1和A5细胞耗竭不会改变通过将GABA注入RVLM或通过静脉注射苯基双胍引起的交感抑制反应，如动脉压和心率降低。这些数据表明，RVLM-C1细胞有助于维持基线动脉压，并在交感兴奋反应中起不可或缺的作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号