It was concluded by Brown and Asbury, that the likely cause of diabetic neuropathy was multi-factoral, with biochemical factors being responsible for early diabetic neuropathy, while actual nerve damage was a consequence of the microangiology of diabetic neuropathy. It was noted that altered rheologic and other variables combined with the effects of microangiopathy would impair nerve blood flow. In recent articles on the pathogenesis of diabetic neuropathy, it was stated that by impairing capillary blood flow, altered blood rheology might be a causal factor in the disorder. The authors of these articles did not , however, advocate the correction of the hemorheological problem to attempt to improve nerve function. Due to the ability of the improved neuromuscular stimulator to achieve maximal muscle recruitment of deep-layered muscles in the peroneal and tibial proximity's, alteration of abnormal hemorheological conditions occurs resulting in measurable and observable effects. Simpson et al drew attention to the possibility that both the early changes in nerve function and the late changes involving endoneurovascular lesions are not explainable in terms of the abnormal flow properties of diabetic blood. Because of the interaction between the abnormal flow properties and the capillary dimension, blood viscosity will increase and may lead to stasis in small endoneural vessels. If irreversible stasis does develop, the result will be a localized region of focal ischemic necrosis with its functional significance being determined by the anatomical location of the lesion. When blood rheology is abnormal, the effects in the microcirculation become so complex that it is difficult to separate cause and effect. Low and Tuck found that increases in or decreases in arterial blood pressure produced comparable changes in the nerve blood flow. They concluded that the blood supply to the peripheral nerve does not tend to autoregulate. They also found that nerve blood flow was reduced by 56% and that vascular resistance increased 85% in rats made hypoxic by breathing oxygen for 10 minutes. When blood rheology was abnormal, oxygen delivery was reduced and capillary blood flow was impaired systemically. Irreversible stasis in the smallest capillaries leading to focal ischemic necrosis would occur during an episode of worsened blood rheology. When blood rheology is improved, damage resulting from the ischemic lesions would be repaired and capillary regeneration would take place. The Poiseuille equation show that the flow rate of Newtonian fluids through narrow tubes is determined by fluid viscosity and the fourth power of the tube radius. Therefore even small differences in tube dimension would give rise to significant changes in flow rate. Since blood is a non-Newtonian fluid, the direct application of the Poiseuille equation is inappropriate, but because of the implications of that formula, it seems that when blood rheology is abnormal, the consequences will be manifested first in the smallest vessels of the microcirculation. Because of this, any study of blood flow in nerve capillaries, the dimensions of endoneural capillaries could be significant. A functional difference in blood supply to muscle and nerve is that muscle is more sensitive to ischemia than nerve. Even though peripheral nerve blood flow may have a significant protective reserve against ischemia, the absence of autoregulation and the apparent lack of lymphatic drainage may render the endoncurim particularly prone to edema. In keeping with the concepts of capillary permeability, increased transudation leading to edema implies increased capillary pressure and/or an increased exposure of basement membrane as a result of the altered disposition of endothelial cell cyoplasm. Due to the physical nature of blood, even the smallest focal reductions in vessel lumen diameter could have hemorheological repercussions. These changes appear to be important in the development of diabetic polyneuropathy.

There are several reasons for believing that oxygen levels determine both the efficiency of nerve function and endoneural blood flow. The following situations are envisaged which parallel some reported studies.

1. When systemic blood pressure is lowered, the rate of endoneural blood flow will be reduced. As a result, thixotrophic amplification of blood viscosity will occur, increasing vascular resistance and thus further reducing the rate of flow of blood. Although in such circumstances oxygen delivery will be enhanced proximally, oxygen tension will be low distally.
2. When systemic blood pressure remains normal but red blood cell deformability is poor, blood flow in the smallest capillaries will be impaired and, in the absence of autoregulation, could lead to stasis and possibly focal neurosis subsequent to anoxia.
3. When systemic blood pressure is raised to overcome the peripheral resistance to abnormally viscous blood, and poorly deformable red blood cells, endoneural blood vessel perfusion pressure will be enhanced. By contracting the muscle with the neuromuscular stimulator and thereby increasing systemic blood pressure, oxygen loading of red blood cells, increasing the rate of nutrient/metabolic waste exchange, hypoxia will be reduced significantly and neural conductivity increased.

EFFECT OF INCREASED RATES OF LYMPHATIC FLUIDS
ON WOUND HEALING ENHANCEMENT

Whatever increases the flow of blood in the veins also aids the lymph flow. Lymph does not flow from a resting limb, but in a muscular activity the rhythmically contracting muscles squeeze out the lymph by exerting external pressure upon the lymph vessels resulting in a considerable flow. The contracting muscle and resultant increase in flow rates enables the lymphatic system to more speedily remove the waste products from the tissues. The effect of increased flow rates of lymphatic fluids upon enhancement of wound healing are to be found within the four functions of the lymph nodes which are:

1. Filtration
2. Formation of lymphocytes
3. Disposal of bacteria
4. Production of antibodies.

BIBLIOGRAPHY

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