Publications (2)4.03 Total impact
-
Article: Protective effects of electroacupuncture on cardiac function in rats subjected to thoracic surgery trauma.
[show abstract] [hide abstract]
ABSTRACT: The present study investigates the protective effects of electroacupuncture (EA) application on cardiac function, while simultaneously exploring the underlying neurobiological mechanisms, in rats that have experienced thoracic surgery-induced stress. Mean arterial and left intraventricular pressures were monitored as indicators of cardiac function. Meanwhile, the immunohistochemistry for c-Fos protein expression and electrophysiology in vitro in brain nuclei, known to regulate cardiac function, provide insights into the effects of EA on the central nervous system. The results show that cardiac function was dramatically suppressed with thoracic surgery trauma, the expression levels of c-Fos in the paraventricular nucleus (PVN) and the rostral ventrolateral medulla (RVLM) significantly increased, the rheobase intensity of the intracellular current injection needed to initiate the action potential decreased, membrane resistance in the PVN neurons significantly increased, and the inductivity of the postsynaptic potentials in the PVN neurons of the surgery-treated rats significantly decreased. EA application at the Neiguan acupoints (PC6) attenuated the decreases in almost all investigated functional parameters of the heart. EA significantly decreased the number of Fos-immunoreactive neurons in the PVN and RVLM, significantly decreased the Max L. slope of the PVN neurons, and increased the inductivity of the postsynaptic potentials in the PVN neurons of the surgery-treated rats. These data indicate the protective effects of EA application on cardiac function in rats that have experienced surgery-induced stress and show that EA application at the Neiguan acupoints may produce its protective effects through the neurons in the PVN and the RVLM.Brain research bulletin 06/2012; 89(1-2):71-8. · 2.18 Impact Factor -
Article: Nitric oxide modulates cardiovascular function in the rat by activating adenosine A2A receptors and inhibiting acetylcholine release in the rostral ventrolateral medulla.
[show abstract] [hide abstract]
ABSTRACT: 1. Nitric oxide (NO), a gas transmitter, modulates many physiological processes, including the central regulation of cardiovascular activity. However, the mechanisms underlying the regulation of cardiovascular activity remain relatively unexplored. In the present study, we hypothesized that central NO-dependent sympathetic inhibition is mediated by activation of adenosine A(2A) receptors (A(2A)R) and inhibition of acetylcholine (ACh) release in the rostral ventrolateral medulla (RVLM). 2. L-Arginine (L-Arg; an NO donor; 100 nmol/100 nL) was microinjected into the RVLM of male Sprague-Dawley rats and heart rate variability (HRV) was assessed as an index of cardiac sympathovagal balance. Following microinjection of L-Arg, decreases were seen in mean arterial pressure (MAP), heart rate (HR) and the ratio of the low- to high-frequency components (LF/HF) of HRV. Pretreatment of rats with SCH58261 (40 pmol/60 nL into the RVLM), a competitive antagonist of the A(2A) R, attenuated these effects. 3. Western blot analysis and ELISA revealed that adenosine and A(2A)R levels increased in the RVLM following L-Arg microinjection, whereas ACh and muscarinic M(1) receptor levels decreased significantly, in parallel with the cardiovascular responses to L-Arg microinjection. The decrease in ACh levels was abolished by SCH58261 pretreatment. 4. Microinjection of N(G)-nitro-L-arginine methyl ester (a non-selective inhibitor of NO synthase; 15 nmol/100 nL) into the RVLM significantly increased MAP, HR and sympathetic activity, as evidenced by HRV (LF, HF and the LF/HF ratio were all increased). 5. The results indicate that the central NO/NO synthase system in the RVLM may modulate cardiovascular activity by activating the A(2A)R, which subsequently inhibits activation of the muscarinic M(1) receptor.Clinical and Experimental Pharmacology and Physiology 03/2011; 38(6):380-6. · 1.85 Impact Factor
