当前位置: X-MOL 学术Brain Res. Bull. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Pilocarpine-induced status epilepticus reduces chemosensory control of breathing.
Brain Research Bulletin ( IF 3.5 ) Pub Date : 2020-05-17 , DOI: 10.1016/j.brainresbull.2020.05.002
Octávio A C Maia 1 , Milene R Malheiros-Lima 1 , Maria A Oliveira 2 , Claudio L Castro 1 , Henrique T Moriya 3 , Wothan Tavares-de-Lima 2 , Ana C Takakura 2 , Thiago S Moreira 1
Affiliation  

One of the possible causes of death in epilepsy is breathing disorders, especially apneas, which lead to an increase in CO2 levels (hypercapnia) and/or a decrease in O2 levels in arterial blood (hypoxemia). The respiratory neurons located in the ventral brainstem respiratory column are the main groups responsible for controlling breathing. Recent data from our group demonstrated respiratory changes in two experimental models of epilepsy, i.e. audiogenic epilepsy, and amygdala rapid kindling. Here, we aimed to evaluate respiratory changes in the classic model of temporal lobe epilepsy induced by intra-hippocampal injection of pilocarpine. Adult Wistar rats with stainless-steel cannulas implanted in the hippocampus region were used. The animals were submitted to pilocarpine injection (2.4 mg/μL, N = 12-15) or saline (N = 9) into the hippocampus. The respiratory parameters analyzed by whole-body plethysmography were respiratory rate (fR), tidal volume (VT) and ventilation (VE). Respiratory mechanics such as Newtonian airway resistance (Rn), viscance of the pulmonary parenchyma (G) and the elastance of the pulmonary parenchyma (H) were also investigated. No changes in baseline breathing were detected 15 or 30 days after pilocarpine-induced status epilepticus (SE). However, 30 days after pilocarpine-induced SE, a significant reduction in VE was observed during hypercapnic (7% CO2) stimulation, without affecting the hypoxia (8% O2) ventilatory response. We also did not observe changes in respiratory mechanics. The present results suggest that the impairment of the hypercapnia ventilatory response in pilocarpine-induced SE could be related to a presumable degeneration of brainstem respiratory neurons but not to peripheral mechanisms.

中文翻译:

毛果芸香碱诱导的癫痫持续状态降低了呼吸的化学感应控制。

癫痫死亡的可能原因之一是呼吸障碍,尤其是呼吸暂停,这会导致 CO2 水平升高(高碳酸血症)和/或动脉血中 O2 水平降低(低氧血症)。位于脑干腹侧呼吸柱的呼吸神经元是负责控制呼吸的主要神经元。我们小组的最新数据证明了两种癫痫实验模型的呼吸变化,即听源性癫痫和杏仁核快速点燃。在这里,我们旨在评估海马内注射毛果芸香碱诱导的经典颞叶癫痫模型的呼吸变化。使用在海马区植入不锈钢套管的成年 Wistar 大鼠。将动物注射毛果芸香碱 (2.4 mg/μL, N = 12-15) 或盐水 (N = 9) 到海马体中。全身体积描记法分析的呼吸参数为呼吸频率 (fR)、潮气量 (VT) 和通气量 (VE)。还研究了呼吸力学,例如牛顿气道阻力 (Rn)、肺实质 (G) 的黏度和肺实质 (H) 的弹性。在毛果芸香碱诱发的癫痫持续状态 (SE) 后 15 或 30 天未检测到基线呼吸的变化。然而,毛果芸香碱诱导 SE 30 天后,在高碳酸血症 (7% CO2) 刺激期间观察到 VE 显着降低,而不会影响缺氧 (8% O2) 通气反应。我们也没有观察到呼吸力学的变化。
更新日期:2020-05-17
down
wechat
bug