Dr. Tom Burke, Ph.D Articles

This is the first in a series of articles that relate specifically to nitric oxide (NO), a free radical gas that is a powerful regulator of circulation (It is an endogenous vasodilator.) and a neurotransmitter (It helps in the processing of nerve signals as they cross synapses.). L-arginine, one of 20 amino acids that make up proteins, is the only amino acid that generates significant amounts of NO. Both circulation and neural function are impaired in diabetic patients, more so if tight glucose control is not maintained.

Diabetic patients are particularly at risk for damage to sensory and motor nerves in the feet or to dysfunction of the autonomic nervous system that innervates internal organs, for example, the intestine. The clinical diagnosis of the latter condition is gastroparesis. NO is an important signaling molecule conveying information from one nerve to another, including non-cholinergic, non-adrenergic (NCNA) nerves. NCNA nerves control smooth muscle cells, which regulate gastric emptying and intestinal motility. Reduced availability of NO in diabetic patients may be one cause of gastroparesis.

Nitric Oxide (NO) offers pain relief in a number of ways. In fact, NO is the mediator of the analgesic effect of opioids such as morphine. In this article we describe how NO affects pain responses and, in particular, certain pain responses in people with diabetes.  

Light-mediated vasodilation was first described by R. F. Furchgott, in his nitric oxide research that led to his receipt of a Nobel Prize in 1998. Later studies conducted by other researchers confirm and extend Furchgott’s early work and demonstrate the ability of light or photo energy to influence the localized production or release of NO and stimulate vasodilation through NO’s effect on cGMP (as discussed in detail in Part Four). This finding suggests that properly designed illumination devices may be effective, noninvasive therapeutic agents for patients who would benefit from increased localized NO availability. 

Use of the Anodyne Therapy System (ATS) appears to elevate NO locally so that blood flow can be increased directly at the site of application. This increase in blood flow is the basis of the therapeutic benefits of the ATS on pain and neuropathy, as we discussed earlier. Recall that arterial AND venous dilation occur in the presence of NO; throughput at the wound site is increased. Wounds such as diabetic ulcers, venous stasis ulcers, and pressure ulcers fail to heal without adequate blood flow to and from the site of injury. The ATS, which certainly increases circulation, might be expected to assist in the healing of wounds for reasons mentioned in Part 10, last week.