Neuronal activity within the ventrolateral periaqueductal gray during simulated hemorrhage in conscious rabbits.

Neuronal activity within the ventrolateral periaqueductal gray during simulated hemorrhage in conscious rabbits.
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清醒兔子模拟出血期间腹外侧导水管周围灰质内的神经元活动。

DOI:
10.1152/ajpregu.00374.2004
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发表时间:
2006
期刊:
American journal of physiology. Regulatory, integrative and comparative physiology
影响因子:
--
通讯作者:
McKown,MichaelD
McKown,MichaelD
中科院分区:
--
文献类型:
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作者:
Schadt,JamesC;Shafford,HeidiL;McKown,MichaelD

文献摘要

相似文献

已经提出腹外侧(vl)导水管周围灰质(PAG)是负责触发低血压发作的主动过程的部位(即,阶段2)(Cavun S和Millington WR.Am J Physiol Regul Integr Comp Physiol 281:R747-R752,2001)。我们记录了清醒家兔PAG神经元的细胞外活动,以验证在模拟出血期间低血压发作之前vlPAG神经元改变其放电频率的假设。在10只家兔体内植入动脉和静脉导管、胸内腔静脉封堵器和微驱动器上的中脑微电极。在模拟出血过程中,封堵器充盈至动脉压≤40 mmHg。我们比较了64个vlPAG和29个背外侧(dl)PAG神经元在模拟出血过程中的神经元活动变化与在类似长度的控制期。动脉压力脉冲调制的神经元活动存在于45和76%的vlPAG和dlPAG神经元,分别。当我们评估活动的绝对变化时,因此考虑到增加和减少,模拟出血对vlPAG而不是dlPAG神经元的活动有显著影响。大多数(56%)vlPAG神经元似乎对模拟出血没有反应。在28个响应性vlPAG神经元中,11个在低血压发作之前的时间间隔期间显示出放电频率的突然变化; 13个在低血压发作之后响应;并且4个在整个模拟出血中显示出一致的变化方向。因此,记录的vlPAG神经元中的24个(38%)在与对与模拟出血相关的低血压的贡献一致的时间响应。
The ventrolateral (vl) periaqueductal gray (PAG) has been proposed as a site responsible for the active process triggering the onset of hypotension (i.e.,phase 2) during blood loss in conscious animals (Cavun S and Millington WR.Am J Physiol Regul Integr Comp Physiol281: R747–R752, 2001). We recorded the extracellular activity of PAG neurons in conscious rabbits to test the hypothesis that vlPAG neurons change their firing frequency before the onset of hypotension during simulated hemorrhage. Arterial and venous catheters, an intrathoracic vena caval occluder, and midbrain microelectrodes on a microdrive were implanted in 10 rabbits. During simulated hemorrhage, the occluder was inflated until arterial pressure ≤40 mmHg. We compared changes in neuronal activity during simulated hemorrhage with those during a similar length control period for 64 vlPAG and 29 dorsolateral (dl) PAG neurons. Arterial pressure pulse modulation of neuronal activity was present in 45 and 76% of vlPAG and dlPAG neurons, respectively. When we evaluated the absolute change in activity, thus accounting for both increases and decreases, simulated hemorrhage had a significant effect on activity of vlPAG but not dlPAG neurons. The majority (56%) of vlPAG neurons did not appear to respond to simulated hemorrhage. Of the 28 responsive vlPAG neurons, 11 showed an abrupt change in firing frequency during the time interval preceding the onset of hypotension; 13 responded after the onset of hypotension; and 4 showed a consistent direction of change across the entire simulated hemorrhage. Thus 24 (38%) of the vlPAG neurons recorded responded at a time consistent with a contribution to the hypotension associated with simulated hemorrhage.