Pulse Width Modulation Electro‐Acupuncture on Cardiovascular Remodeling and Plasma Nitric Oxide in Spontaneously Hypertensive Rats
Author(s) -
Xuan Xiong,
Chao You,
Qiu-Chao Feng,
Ting Yin,
Chen Zhong-ben,
Patrick Ball,
Lexin Wang
Publication year - 2010
Publication title -
evidence-based complementary and alternative medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.552
H-Index - 90
eISSN - 1741-4288
pISSN - 1741-427X
DOI - 10.1093/ecam/neq063
Subject(s) - captopril , ventricle , medicine , nitric oxide , endocrinology , pulse (music) , blood pressure , acupuncture , cardiology , alternative medicine , pathology , detector , electrical engineering , engineering
This study was designed to investigate the effect of pulse width modulation electro-acupuncture (PWM-EA) on cardiovascular remodeling and nitric oxide (NO) in spontaneously hypertensive rats (SHR). Thirty-four male SHR were randomly divided into control, captopril, and two PWM-EA groups, which were treated with 350 Hz (SHR-350 Hz) and whole audio bandwith electro-acupuncture (SHR-WAB group) respectively, on the ST 36 point located on the outside of the hind leg. Systolic blood pressure (BP), plasma and myocardial NO were measured. Histological studies were also performed on the aortic wall and the left ventricle. The BP in the SHR-350 Hz, SHR-WAB and the captopril groups was lower than in the control group following the treatment ( P < .05). The average aortic media wall thickness in the two electro-acupuncture groups was less than in the control group ( P < .05). The left ventricle/heart weight ratio in the captopril and SHR-350 Hz groups was less than in the control group ( P < .01), but was similar between the SHR-WAB and the control group ( P > .05). The plasma and myocardium NO levels were elevated in the captopril and the SHR-350 Hz group ( P < .05 and .01, resp.). The plasma level of NO in the SHR-WAB group was also higher than in the control group ( P < .05). We concluded that pulse width modulation electro-acupuncture on the ST 36 point prevents the progression of hypertension and diminishes the cardiovascular remodeling in SHR. It also elevates plasma and cardiac NO in this animal model.
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