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To test the hypothesis of a myofascial component in intermittent claudication, 56 male patients were studied. Calf blood flow, at rest and during postischemic and postexercise hyperemia, presence of trigger areas, and exercise tolerance were evaluated and compared. The results can be summarized as follows: The exercise tolerance is reduced when trigger areas are present in the calf muscles, and the more severe the trigger areas, the lower is the exercise tolerance. Trigger areas are more severe when the hyperemic flow is more reduced. The peak flow of reactive hyperemia is also correlated to work load. Pain in intermittent claudication is a complex phenomenon. According to the aforesaid results, the severity of limb ischemia and the presence of trigger areas in the calf appear to be the major factors. Besides the two reasons already known, a third is suggested to explain calf claudication: the elective location of trigger points in the gastrocnemius muscle.

Twenty patients with peripheral arterial disease and 10 normal controls were submitted to i.v. injection of aprotinin, polypeptide (mol.wt. 6512) extracted from bovine lung, in order to examine its effects on: (a) lower limbs pain, (b) lower limbs sensibility, (c) calf blood flow. Aprotinin (100,000 Ku i.v. diluted in NaCl 0.9%) was given in a single dose or twice a day for a week; for control the same subject received, before or after aprotinin, an equivalent volume of diluent (0.9% NaCl). The results demonstrate that aprotinin is able to increase the initial pain limit walking tolerance and to decrease the intensity of pain at rest and of myalgic or "trigger" areas. No variation was observed on skin sensibility and on calf blood flow, both basal resting and hyperemic. The favorable effect of examined polypeptide on ischemic pain can be attributed neither to increase of calf blood flow nor to influence on perception of painful stimuli. It seems therefore to suggest that aprotinin acts on biochemical mechanisms that cause the ischemic pain. Presumably it inhibits kininogenases and tissue protein-hydrolyzine enzymes activated in the course of ischemia.

Blood flow in the calf was measured during postexercise hyperemia in normal subjects and in PAD patients by means of a foot ergometer that gives direct reading of the work performed. In normals, first and peak flow increased with the rise of work load up to 100 KGM. The duration of hyperemia increased with a work load of 30 to 200 KGM. In PAD patients, first flow did not coincide with peak flow. Peak flow was lower and delayed, and the duration of hyperemia was more prolonged than in normal subjects. In patients with intermittent claudication, first flow, peak flow, and work load were higher than in patients with rest pain or impending gangrene. Exercise hyperemia appears as a useful test for screening normal limbs from those with arterial obstruction. Since in PAD patients exercise is interrupted when muscular pain appears, it is evident that the earlier the arrest of work and the appearance of pain, the greater is the involvement in the arterial tree of the leg. Therefore the exercise hyperemia test can be used also as a means of evaluating the different stages of PAD.

Reactive and exercise hyperemia were compared in healthy men and in patients with PAD. In both patients and normals the calf blood flow of reactive hyperemia was recorded after a 5-minute ischemia. Exercise hyperemia was measured in normals after variable work loads (30 and 50 kg) and immediately after the occurrence of pain in patients with PAD. In healthy limbs the first and peak flows of exercise and reactive hyperemia are similar. The recovery time for basal flow is prolonged after exercise. However, reactive and exercise hyperemia differ significantly when arterial obstruction due to arteriosclerosis obliterans is present. First flow and peak flow are higher and recovery time more prolonged after exercise. It is also likely that the control mechanisms of the two hyperemic reactions are different. Muscular exercise, when protracted until pain occurs, can produce a metabolic and circulatory adjustment other than that of ischemia. There is experimental evidence to support this hypothesis.

The relationships between blood rheology and peripheral arterial disease are reviewed. The connections between abnormal blood rheology and peripheral arterial disease are discussed considering the opinions of the enthusiastic and skeptic rheologists. A prospective for future investigations is also proposed.

Reactive hyperemia was studied by plethysmographic measurement of the blood flow in the calf in normal subjects and in patients with peripheral arterial disease following circulatory arrest for periods ranging between 1 and 20 minutes. The duration of occlusion is an important factor in determining the behaviour of reactive hyperemia. Peak flow increases significantly when there is up to 10 minutes of circulatory arrest. Following release of an occlusion of 15 or 20 minutes, the further rise of peak flow is very moderate. The duration of subsequent hyperemia is greater in patients than in normal subjects, when the length of the occlusion is of 1 to 10 minutes. When circulatory arrest is prolonged for more than 10 minutes, the recovery time of basal flow is significantly greater in normal subjects. Several mechanisms are involved in reactive hyperemia; their relative importance may vary with the duration of occlusion. Circulatory arrest of 3--5 minutes is a useful clinical test to screen patients with arterial occlusive disease. It is not the best for a full evaluation of the blood flow in the lower limbs either in normal subjects or in partients.