In diabetics, clotting factors, as mentioned previously, are greatly increased with platelets having an increased tendency toward adherence and aggregation which, some researchers say, may contribute to the incidence of arteriosclerosis. Information suggests that abnormal platelet adhesiveness and aggregation may be critical factors in the genesis of vascular lesions and microthrombi. This tendency toward increased platelet aggregation may be critical factors in the genesis of vascular lesions and microthrombi. This tendency toward increased platelet aggregation in the diabetic has been attributed to the presence of a plasma factor that potentates ADP-induced platelet aggregation. This factor has been termed PLATELET AGGREGATION ENHANCING FACTOR and has been demonstrated by Kwaan et al, in approximately 50% of the diabetic patients tested. The presence of abnormal levels of platelet aggregates can cause intermittent inversion phenomenon in capillaries and small veins. In this inversion of the Fahreaus-Lindquest phenomenon, there is a sudden and dramatic increase in the resistance to flow and an increase in the viscosity of blood which is caused by the effect platelet aggregates have on the critical radius of capillaries. Even small changes in the rigidity of red blood cells would be greatly magnified by the amplification mechanism of the inversion phenomenon is small vessels which lead to increased resistance to flow and apparent vasoconstriction. Aggregation of red cells might also have a role to play in the inversion phenomenon, especially if compact and sludge-like aggregates of the type observed in cancer or infarction are present.

Jonason et al. Demonstrated the beneficial effects of a supervised training and exercise program in patients with intermittent claudication. Some of this improvement may be attributed to the effect of exercise on platelets. Peterson demonstrated that the percentage of platelet adhesiveness in diabetic subjects fell from 74% before exercise to 53% after exercise. In this study of diabetic patients, the decreased platelet adhesion was maintained at nine hours after exercise in one subject and at 24 hours after exercise in another.

Changes in hemorheological properties of blood can produce changes in flow that are independent of changes in pressure. For example, a decrease in plasma viscosity can produce and increase in blood flow and tissue oxygenation even though pressure may remain constant. In other words variables other than pressure or pressure differentials must be employed to evaluate changes in flow because of hemorheological alterations. A major factor determining blood viscosity is the ability of the red blood cells to aggregate. These large aggregates of red blood cells, which form rouleaux formations, significantly decrease blood flow. Several factors have been demonstrated to enhance red blood cell aggregation.

An increase in the hematocrit, or red blood cells as a percentage of whole blood, increases aggregation. The velocity of blood flow also has an inverse correlation with viscosity which is demonstrated by Poiseuille's Law. As velocity decreases, the natural tendency for aggregation stimulates rouleaux formations, leading to increased viscosity. Another factor determining viscosity is, as previously mentioned, red blood cell deformability. As the velocity of flow increases, red blood cells orient themselves with the direction of the flow and take an ellipsoidal shape with the red blood cell membrane rotating around the cell contents like the caterpillar tread of a tank. Both of these actions enhance blood flow by reducing viscosity. At the capillary level, a major determinant of flow is red blood cell deformability. Some factors tat determine RBC deformability are viscosity of the cell contents, surface area to volume ratio, and flexibility of the cell membrane. It has also been found that alterations in pH level, red blood cell adenosine triphosphate content, and concentrations of metabolic end products alter the membrane skeleton and thus red blood cell deformability.

The flexibility of red blood cells influences blood viscosity through the effect on streamlines in flow. Because normal RBC's change into ellipsoids which conform to the flow patterns, a minimal perturbation of streamlines occurs. Studies using chemically stiffened RBC's have shown that the less deformable the cell, the greater the disturbance of streamlines in flow and the higher the shear rate of viscosity. Flow problems in capillaries occurs by poorly deformable RBC's having diameters larger than that of the capillaries. If intracapillary pressure does not rise sufficiently to cause the stiffened red blood cells to deform, flow will resume, but transudation will be enhanced. If the transudation rate exceeds the lymphatic drainage rate, tissue fluid will accumulate and frank edema will develop. By increasing the rate of flow of blood the red blood cell rigidity will be decreased due to the prevention or retardation of hypoxia which is a major cause of red blood cell rigidity.

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