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大鼠孤束核的化学感觉控制。

Chemosensory control by commissural nucleus of the solitary tract in rats.

机构信息

Department of Physiology and Pathology, School of Dentistry, São Paulo State University (UNESP), Araraquara, SP, Brazil.

出版信息

Respir Physiol Neurobiol. 2011 Dec 15;179(2-3):227-34. doi: 10.1016/j.resp.2011.08.010. Epub 2011 Aug 23.

Abstract

The commissural nucleus of the solitary tract (commNTS) is a main area that receives afferent signals involved in the cardiovascular and respiratory control like those related to chemoreceptor activation, however, the importance of the commNTS for the cardiorespiratory responses to chemoreceptor activation is still controversial. In the present study, we investigated the cardiorespiratory responses to hypoxia or hypercapnia in anesthetized and conscious rats treated with injections of the GABA-A agonist muscimol into the caudal portion of the commNTS. Male Holtzman rats (280-300 g) were used. In conscious rats that had a stainless steel cannula previously implanted into the commNTS, the injection of muscimol (2 mM) into the commNTS reduced the pressor response (16±2 mmHg, vs. saline: 36±3 mmHg) and the increase in ventilation (250±17 ml/min/kg, vs. saline: 641±28 ml/min/kg) produced by hypoxia (8-10% O(2)). In urethane anesthetized rats, the injection of muscimol into the commNTS eliminated the pressor response (5±2 mmHg, vs. saline: 26±5 mmHg) and the increase in phrenic nerve discharge (PND) (20±6%, vs. saline: 149±15%) and reduced the increase in splanchnic sympathetic nerve discharge (sSND) (93±15%, vs. saline: 283±19% of baseline) produced by hypoxia. However, muscimol injected into the commNTS did not change hypercapnia (8-10% CO(2)) induced pressor response or the increase in the sSND or PND in urethane anesthetized rats or the increase in ventilation in conscious rats. The present results suggest that the cardiorespiratory responses to hypoxia are strongly dependent on the caudal portion of the commNTS, however, this area is not involved in the responses to hypercapnia.

摘要

孤束核的连合核(commNTS)是接收涉及心血管和呼吸控制的传入信号的主要区域,例如与化学感受器激活相关的信号,但 commNTS 对于化学感受器激活引起的心肺反应的重要性仍存在争议。在本研究中,我们在麻醉和清醒大鼠中研究了向 commNTS 的尾部注射 GABA-A 激动剂 muscimol 后对缺氧或高碳酸血症的心肺反应。使用雄性 Holtzman 大鼠(280-300g)。在先前将不锈钢套管植入 commNTS 的清醒大鼠中,向 commNTS 内注射 muscimol(2mM)可降低缺氧(8-10%O2)引起的升压反应(16±2mmHg,与盐水相比:36±3mmHg)和通气增加(250±17ml/min/kg,与盐水相比:641±28ml/min/kg)。在乌拉坦麻醉大鼠中,向 commNTS 内注射 muscimol 消除了升压反应(5±2mmHg,与盐水相比:26±5mmHg)和膈神经放电(PND)的增加(20±6%,与盐水相比:149±15%),并减少了缺氧引起的内脏交感神经放电(sSND)的增加(93±15%,与盐水相比:283±19%基线)。然而,向 commNTS 内注射 muscimol 并没有改变麻醉大鼠高碳酸血症(8-10%CO2)引起的升压反应或 sSND 或 PND 的增加,也没有改变清醒大鼠的通气增加。本研究结果表明,缺氧引起的心肺反应强烈依赖于 commNTS 的尾部,但该区域不参与高碳酸血症的反应。

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