THE diversity of opinion regarding the value of the numerous forms of therapy in current use for peripheral vascular disease, we believe, is due to the inadequacy of the tests of circulatory function so far utilized.Walking is a reliable quantitative test of function if judged on the basis of capacity to walk until pain occurs. It is an easily repeated measurement of tolerance and is capable of standardization. It does not involve the use of special apparatus, and it tests muscles that the average elderly patient is accustomed to using -in other words, it constitutes a normal activity for the patients concerned.Chronic progressive occlusion of the vascular supply to an extremity proceeds in three stages : the long preliminary period free of symptoms, except perhaps absence of pulsations in the dorsalis pedis artery; the interval of intermittent claudication, when the blood flow has been reduced by fully two thirds,1 which continues for months or years until further substantial reduction in blood supply is obtained; and the final period, which is characterized by trophic disturbances in the skin, rubor and, eventually, skin infection.The patient usually seeks relief in the second stage. Therapy is generally intended to promote improvement in the circulation of the muscles by vasodilating or other agents, which act presumably by encouraging an increased flow in the collateral vessels. Since the vascular supply to the skin stems from the deep (muscular) vessels, postponement of the superficial-tissue breakdown that leads to gangrene and amputation may be achieved. Measurement of an increase in the circulation of the deep vessels is not directly appraised by the methods in common use. The oscillometer measures pulsations in the large vessels. The plethysmograph cannot be easily adapted for routine clinical study. The muscle-temperature thermocouple is not useful for the measurement of the necessarily slow improvement that may occur. Skintemperature measurements and immersion calorimetry deal essentially with changes in superficial vessels, and there is much evidence to indicate a dissociation in the response of deep and superficial vessels to drugs.2The therapeutic agent tested in this study for its effect on circulatory function was testosterone propionate. The drug was first suggested by Arndt8 in 1939 for the relief of intermittent claudication. This author describes a favorable effect on this condition in 6 men, but the evaluation was based entirely on a general statement by the patient that he felt better. The duration of improvement was not given, and in 2 patients smoking was decreased or eliminated during the period of treatment. Subsequently, Edwards et al.4 reported that testosterone produced "marked improvement in the walking ability of all the patients, with delay or abolition of the intermittent claudication." The patients were followed for several months, but no mention was made of other therapeutic procedures that may have been used simultaneously, nor was any objective measure of evaluation used.In o...

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The effect of smoking upon the blood flow of a sympathectomized limb was examined in 19 patients. Sympathectomy was found to abolish the peripheral vasoconstriction produced by smoking. The constriction, therefore, is mediated by sympathetic vasomotor fibers and not by humoral agents such as adrenaline or posterior pituitary hormone. There is no difference in the response of patients sympathectomized for thromboangiitis obliterans, arteriosclerosis or severe vasospasm. The relation between the vasoconstrictor effect of smoking and the action of tobacco in thromboangiitis obliterans is discussed.T HE PERIPHERAL vasoconstriction produced by smoking has been known for many years. Most investigatorsl-5 have found this constriction due to the action of the absorbed nicotine; and not, as some have claimed, 6,7 the result of sympathetic reflexes initated by the breathing pattern of smoking or by the irritation of the smoke itself. GoetzO reported that the constriction at the very onset of smoking is of such reflex origin, while the more marked decrease in blood flow which follows is due to the sympathomimetic action of the absorbed nicotine.Nicotine in the amount inhaled from one or two cigarettes acts as a general synaptic stimulant. As such, in theory, it could produce peripheral vasoconstriction by four known mechanisms: (1) by the excitation of central vasomotor centers, (2) by a direct stimulation of sympathetic ganglia, (3) by an increased production of adrenaline, and (4) by the liberation of posterior pituitary hormone. The first two of these mechanisms require an intact sympathetic nerve supply to the blood vessels. The third and fourth are humoral and should not be abolished by sympathectomy. Rather,

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