Responses of the Human Upper Extremity Vascular Bed to Exercise, Cold, Levarterenol, Angiotensin, Hypertension, Heart Failure, and Respiratory Tract Infection with Fever *

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Abstract
Pressures were measured at 4 sites along the length of the vascular bed in the human upper extremity. These sites included the brachial artery, the radial artery or one of its branches, a vein on the dorsum of the hand or proximal phalanx, and a vein in or near the antecubital space. Ex-tremity blood flow was estimated by an indicator-dilution method. In essential and renal hypertension, the pressure gradient from small artery to small vein was elevated. The pressure gradients from brachial artery to small artery and from small vein to antecubital vein were normal. These findings suggest that the elevated peripheral resistance results from constriction of the smaller vessels. Congestive heart failure decreased the rate of blood flow by increasing the resistance to flow. Since the hematocrit was low, the increase in resistance results from vascular constriction. Antecubital vein pressure rose more than small vein pressure. The decrease in the venous pressure gradient was about in proportion to the decrease in flow. Venous resistance was, therefore, not elevated, suggesting that the vascular constriction is upstream to the small vein and compliance of the veins is low. Elevation of small vein pressure (and, by inference, capillary hydrostatic pressure) apparently results both from rise of right atrial pressure and decrease of venous compliance. Respiratory tract infection with fever increased the rate of blood flow through upper extremity by decreasing the resistance to flow. Since the hematocrit was often elevated, the decrease in resistance results from vascular dilation. Change in position did not affect venous pressure, but exercise increased small vein pressure in normal subjects and in patients with compensated heart disease. This finding suggests that the loss in plasma volume during exercise results from elevation of capillary hydrostatic pressure. In resting subjects, small vein pressure was spontaneously more variable than antecubital vein pressure. In normal subjects, intrabrachial injection of levarterenol or angiotensin produced a transient fall in small vein pressure followed by a relatively sustained rise above the control value. Subcutaneous tissue temperature in the area of the small vein started falling shortly after injection and remained low during the pressor phase. Acetylcholine produced only a rise in pressure. Exposure of the hand or the hand and forearm to cold produced a slow large rise in small vein pressure.