Dental School of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, 14040-904, Brazil.
Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, 14049-900, Brazil.
J Neuroinflammation. 2019 Jun 20;16(1):125. doi: 10.1186/s12974-019-1512-6.
Lipopolysaccharide (LPS)-induced systemic inflammation (SI) is associated with neuroinflammation in the brain, hypotension, tachycardia, and multiple organs dysfunctions. Considering that during SI these important cardiovascular and inflammatory changes take place, we measured the sensitivity of the cardiovascular reflexes baroreflex, chemoreflex, and Bezold-Jarisch that are key regulators of hemodynamic function. We also evaluated neuroinflammation in the nucleus tractus solitarius (NTS), the first synaptic station that integrates peripheral signals arising from the cardiovascular and inflammatory status.
We combined cardiovascular recordings, immunofluorescence, and assays of inflammatory markers in male Wistar rats that receive iv administration of LPS (1.5 or 2.5 mg kg) to investigate putative interactions of the neuroinflammation in the NTS and in the anteroventral preoptic region of the hypothalamus (AVPO) with the short-term regulation of blood pressure and heart rate.
LPS induced hypotension, tachycardia, autonomic disbalance, hypothermia followed by fever, and reduction in spontaneous baroreflex gain. On the other hand, during SI, the bradycardic component of Bezold-Jarisch and chemoreflex activation was increased. These changes were associated with a higher number of activated microglia and interleukin (IL)-1β levels in the NTS.
The present data are consistent with the notion that during SI and neuroinflammation in the NTS, rats have a reduced baroreflex gain, combined with an enhancement of the bradycardic component of Bezold-Jarisch and chemoreflex despite the important cardiovascular impairments (hypotension and tachycardia). These changes in the cardiac component of Bezold-Jarisch and chemoreflex may be beneficial during SI and indicate that the improvement of theses reflexes responsiveness though specific nerve stimulations may be useful in the management of sepsis.
脂多糖(LPS)诱导的全身炎症(SI)与大脑中的神经炎症有关,表现为低血压、心动过速和多个器官功能障碍。考虑到在 SI 期间会发生这些重要的心血管和炎症变化,我们测量了心血管反射的敏感性,包括压力反射、化学反射和 Bezold-Jarisch 反射,它们是调节血液动力学功能的关键调节者。我们还评估了孤束核(NTS)中的神经炎症,NTS 是整合心血管和炎症状态引起的外周信号的第一个突触站。
我们结合心血管记录、免疫荧光和炎症标志物检测,对接受 LPS(1.5 或 2.5mg/kg)静脉注射的雄性 Wistar 大鼠进行研究,以研究 NTS 和下丘脑前腹侧视前区(AVPO)中的神经炎症与短期血压和心率调节之间的潜在相互作用。
LPS 诱导低血压、心动过速、自主神经失衡、低温后发热以及自发性压力反射增益降低。另一方面,在 SI 期间,Bezold-Jarisch 的心动过缓成分和化学反射的激活增加。这些变化与 NTS 中激活的小胶质细胞数量增加和白细胞介素(IL)-1β水平升高有关。
本研究数据表明,在 SI 和 NTS 神经炎症期间,大鼠的压力反射增益降低,同时 Bezold-Jarisch 和化学反射的心动过缓成分增强,尽管存在重要的心血管损伤(低血压和心动过速)。Bezold-Jarisch 和化学反射的心脏成分的这些变化在 SI 期间可能是有益的,并且表明通过特定的神经刺激来改善这些反射的反应性可能有助于脓毒症的管理。