Exogenous nitric oxide centrally enhances pulmonary reactivity in the normal and hypertensive rat
Exogenous nitric oxide centrally enhances pulmonary reactivity in the normal and hypertensive rat
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DOI：
10.1111/j.1440-1681.2005.4290.x
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发表时间：
2005-11
影响因子：
2.9
通讯作者：
D. Schwenke;J. Pearson;H. Tsuchimochi;H. Mori;M. Shirai
中科院分区：
文献类型：
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作者：
D. Schwenke;J. Pearson;H. Tsuchimochi;H. Mori;M. Shirai
1.慢性缺氧导致持续性肺动脉高压，虽然肺内皮一氧化氮（NO）通路的损害已牵连，没有研究已经描述了NO在调节肺血管张力和反应性的核心作用。在中枢，NO抑制交感神经流出，因此我们假设，中枢NO将调节肺血管张力及其对急性缺氧的反应性，特别是在高血压状态下。
1. Chronic hypoxia causes sustained pulmonary hypertension and, although impairment of the pulmonary endothelial nitric oxide (NO) pathway has been implicated, no study has described the central role of NO in modulating pulmonary vascular tone and reactivity. Centrally, NO inhibits sympathetic outflow, so we hypothesised that central NO would modulate pulmonary vascular tone and its reactivity to acute hypoxia, especially in the hypertensive state.