A Neurovascular Transmission Model for Acupuncture-induced Nitric Oxide

Abstract

Acupuncture is the practice of inserting needles into the body to reduce pain or induce anesthesia. More broadly, acupuncture is a family of procedures involving the stimulation of anatomical locations on or in the skin by a variety of techniques. Employing acupuncture to treat human disease or maintain bodily condition has been practiced for thousands of years. However, the mechanism(s) of action of acupuncture at the various meridians are poorly understood. Most studies have indicated that acupuncture is able to increase blood flow. The acupuncture points have high electrical conductance and a relationship of the acupuncture points and meridians with the connective tissue planes and the perivascular space has also been suggested. Several studies employing the human and animal models have shown that acupuncture enhances the generation of nitric oxide (NO) and increases local circulation. Specifically, electroacupuncture (EA) seems to prevent the reduction in NO production from endothelial NO synthetase (eNOS) and neuronal NO synthase (nNOS) that is associated with hypertension and this process involves a stomach-meridian organ but not a non-stomach-meridian organ such as the liver. How can we explain the phenomena of EA and meridian effect? Here, we proposed a neurovascular transmission model for acupuncture induced NO. In this proposed model, the acupuncture stimulus is able to influence connective tissue via mechanical force transfer to the extracellular matrix (ECM). Through the ECM, the mechanotransduction stimulus can be translated or travel from the acupuncture points, which involve local tissue and cells. Cells in the local tissue that have received mechanotransduction induce different types of NO production that can induce changes in blood flow and local circulation. The local mechanical stress produced is coupled to a cyclic strain of the blood vessels and this could then change the frequency of resonance. According to the resonance theory, an oscillatory pattern of NO formation might occur in that specific organ. Therefore, the artery tree would then change the blood distribution and microcirculation of various organs and as a result further affect the production of NO.

Acupressure at the Meridian Acupoint Xiyangguan (GB33) Influences Near-Infrared Spectroscopic Parameters (Regional Oxygen Saturation) in Deeper Tissue of the Knee in Healthy Volunteers

“…It has also been suggested that cyclic Guanosine Monophosphate (cGMP) mediates the signaling functions of nitric oxide (NO) to improve local microcirculation [21]. A neurovascular transmission model for the acupuncture-induced NO effect has been proposed by Hsiao and Tsai [22]. In this model, the acupuncture stimulus is able to influence connective tissue via mechanical force transfer to the extracellular matrix (ECM).…”

Electroacupuncture improves recovery after hemorrhagic brain injury by inducing the expression of angiopoietin-1 and -2 in rats

“…Several studies have shown that NO can upregulate Ang-1 expression after stroke, and the effects of inflammatory cytokines on the expression of Ang-1 and Ang-2 depend on their concentration: high concentrations of cytokines result in negative expression of Ang-1 and Ang-2, while low concentrations of cytokines result in positive expression of Ang-1 and Ang-2 [30-33]. Furthermore, EA can upregulate the NO level [34] and have an anti-inflammatory effect after stroke [35]. Accordingly, it is tempting to suppose that EA at the Zusanli (ST36) acupoint regulates the expression of Ang-1 and Ang-2 by increasing the NO level and decreasing inflammation.…”

Electroacupuncture treatment contributes to the downregulation of neuronal nitric oxide synthase and motoneuron death in injured spinal cords following root avulsion of the brachial plexus

“…In a rabbit model of hepatic ischemia-reperfusion injury, EA at Yanglingquan (GB34) inbibited the production of iNOS in the liver, reduced the content of nitric oxide (NO) and malondialdehyde (MDA) and increased the activity of superoxide dismutase (SOD) (30). Likewise, in a rat model of streptozocin-induced Alzheimer's disease, a PD rat model, a hypothalamus of spontaneously hypertensive rats model, a cerebral ischemia-reperfusion injury rat model and a rabbit model of knee osteoarthritis, EA played pivotal roles on reducing oxidative stress by raising the content of SOD, lowering MDA or NO and even changing the blood distribution and microcirculation of various organs (31)(32)(33)(34)(35). Notably, EA affected the levels of SOD and MDA in different organs in a hyperlipemia rat model (36).…”