Relationship between sympathetic activity and arterial pressure in conscious spinal rats
Relationship between sympathetic activity and arterial pressure in conscious spinal rats
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DOI：
10.1152/ajpheart.1997.272.2.h625
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发表时间：
1997-02-01
影响因子：
4.8
通讯作者：
Krassioukov, AV
中科院分区：
文献类型：
--
作者：
Maiorov, DN;Weaver, LC;Krassioukov, AV
脊髓损伤会扰乱动脉压的调节，常常导致由脊髓反射引发的阵发性高血压。脊髓产生的交感神经活动（SNA）对脊髓损伤后静息动脉压控制的贡献值得怀疑。反射性高血压的机制也尚未解决。一个重要的问题是，这种高血压是否是由大的脊髓交感反射引起的，还是由已知的血管对去甲肾上腺素的敏感性增加以及脊髓损伤后发生的压力感受器反射的有效性有限引起的。我们评估了清醒大鼠在胸中部脊髓横断（SCT）后 1 周的基础条件和结肠扩张引起的反射性加压反应期间肾 SNA 与平均动脉压（MAP）之间的关系。 SCT后一天，相同麻醉大鼠的MAP（69±6mmHg）和SNA（6±2μV·s）低于SCT前的MAP（92±4mmHg）和SNA（18±3μV·s）。第 6 天，MAP 增加至 94 +/- 6 mmHg，而 SNA 仍然较低（4 +/- mu V.s）。 SCT 后一天，结肠扩张使 MAP 增加 28 +/- 4 mmHg，SNA 增加 35 +/- 6 muV。 s;这些答复在 6 天内保持不变。这些数据表明脊髓产生的 SNA 对基础 MAP 没有明显的贡献。相反，传入刺激可以产生大量的兴奋性脊髓交感神经反射，足以导致动脉压大幅升高。
Spinal cord injury disrupts regulation of arterial pressure, often resulting in episodic hypertension initiated by spinal reflexes. The contribution of spinally generated sympathetic nerve activity (SNA) to control of resting arterial pressure after cord injury is questionable. The mechanisms responsible for the reflex hypertension also are unresolved. One important question concerns whether or not this hypertension is caused by large spinal sympathetic reflexes or by the known increased vascular sensitivity to norepinephrine and limited effectiveness of baroreceptor reflexes that occur after spinal cord injury. We evaluated the relationship between renal SNA and mean arterial pressure (MAP) in basal conditions and during reflex presser responses induced by colon distension in conscious rats for 1 wk after midthoracic spinal cord transection (SCT). One day after SCT, MAP (69 +/- 6 mmHg) and SNA (6 +/- 2 mu V . s) were lower than the MAP (92 +/- 4 mmHg) and SNA (18 +/- 3 mu V . s) in the same anesthetized rats before SCT. At 6 days, MAP increased to 94 +/- 6 mmHg, whereas SNA remained low (4 +/- mu V . s). One day after SCT, colon distension increased MAP by 28 +/- 4 mmHg and SNA by 35 +/- 6 mu V . s; these responses remained unchanged for 6 days. These data suggest that spinally generated SNA makes no apparent contribution to basal MAP. In contrast, afferent stimulation can produce large excitatory spinal sympathetic reflexes that appear adequate to cause substantial increases in arterial pressure.