Apelin in the hypothalamic paraventricular nucleus improves cardiac function in surgical trauma rats
- Author:
- No author available
- Journal Title:
- Acta Physiologica Sinica
- Issue:
- 2
- DOI:
- 10.13294/j.aps.2018.0026
- Key Word:
- apelin;手术创伤;室旁核;延髓头端腹外侧区;电针;apelin;surgical trauma;paraventricular nucleus;rostral ventrolateral medulla;electro-acupuncture
Abstract： Apelin is a novel endogenous active peptide.The aim of this study is to investigate whether apelin in the paraventricular nucleus (PVN) can improve the cardiac function in rats subjected to thoracic surgery trauma,and whether it is involved in the protective effect of electro-acupuncture (EA).Sprague-Dawley rats were randomly divided into non-stressed group (control),thoracic surgical trauma stressed group (trauma) and bilateral Neiguan EA applied on thoracic surgical trauma stressed group (trauma + EA-PC 6).The mRNA expressions of apelin receptor (APJR) and apelin in the PVN were detected by real time-PCR.The exogenous apelin-13 (6 mmol/L,0.1 μL) was microinjected into the rat PVN in the thoracic trauma group,and the effects of apelin-13 on the blood pressure (BP),heart rate (HR) and the discharge of rostral ventrolateral medulla (RVLM) neurons were observed through the simultaneous recording technology by polygraph.The results showed that the APJR mRNA expression was significantly decreased in the rats of trauma group as compared with that in the control group (P ＜ 0.05),and a decline trend of apelin mRNA expression was also observed.EA application at bilateral Neiguan acupoints partially recovered the decline of APJR and apelin mRNA expression by the treatment of thoracic trauma.Both mean arterial pressure and HR in the thoracic surgical trauma group were significantly increased by the microinjection of exogenous apelin-13 into the PVN (P ＜ 0.05),and the single-unit discharge rate of RVLM neurons also had an increasing trend.These results suggest that apelin in the PVN can improve the cardiac function of thoracic surgical trauma rats,and may be involved in the protective effects of EA.
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