Blood Flow in the Hand and Forearm after Paravertebral Block of the Sympathetic Ganglia. Evidence against Sympathetic Vasodilator Nerves in the Extremities of Man.

Many of the blood vessels of the extremities are under reflex control. Numerous stimuli, such as cooling the body, pain, loud noise, or deep inspiration, produce reflex vasoconstriction. Heating the body causes reflex vasodilatation. The fact that either preor post-ganglionic sympathectomy eliminates these vasoconstrictor and vasodilator responses demonstrates that the sympathetic nerves contain the efferent limb of the reflex arc for both types of response (1, 2). These vasomotor reflexes which are mediated through the sympathetic nerves could be explained equally well by either of the following hypotheses: (a) that vasoconstriction is an active process resulting from reflex sympathetic stimulation, and vasodilatation is a passive phenomenon resulting from inhibition or lack of sympathetic activity; (b) that both vasoconstriction and vasodilatation are active processes resulting from reflex activity. The latter hypothesis assumes that part of the reflex vasodilatation results from inhibition of active vasoconstriction, but that vasodilatation beyond that point is an active process resulting from reflex stimulation of the vasodilator nerves. This hypothesis gained support from the demonstration that the sympathetic nerves to the extremities contain both adrenergic and cholinergic fibers. The nerves supplying the sweat fibers are cholinergic, but anatomically they form a part of the sympathetic system. Might it not be possible that vasodilator, cholinergic fibers also coursed through the sympathetic ganglia and nerves? Lewis and Pickering observed that heating the body was the most satisfactory means of causing neurogenic vasodilatation in the extremities of both normal subjects and patients with Raynaud's disease, and that this response to body heating occurred only in the presence of intact sympathetic innervation (1). They noted that in normal subjects whose skin temperature had previously been lowered by exposure in a cold room, blocking the ulnar nerve caused vasodilatation and warming of the anesthetized fingers. In two of their patients with Raynaud's disease, block of the ulnar nerve did not cause the fourth and fifth fingers to warm. Heating the body produced normal vasodilatation in these fingers. They concluded: "To sum up, it is found in cases of Raynaud's disease exposed to suitable room temperature that ulnar anesthesia, with its inhibition of vasoconstrictor tone, fails to release the vascular spasm, but that under the same conditions, warming the body relaxes the vessels. The last effect occurs through sympathetic paths, failing to occur after sympathectomy, but as it is not due to simple inhibition of vasoconstrictor tone, being, in fact, prevented by anesthetization of the mixed nerve, it must be attributed to active vasodilatation." These experiments are not conclusive because no evidence was obtained to show that the block of the ulnar nerve had actually inhibited the vasoconstrictor impulses to the vessels supplying the fourth and fifth fingers. It has been found that it is not always safe to rely on anesthesia alone as a sign that all sympathetic fibers to the area are blocked (3). Lewis and Pickering (1), estimating changes in blood flow from changes in skin temperature, were unable to obtain evidence of vasodilator nerves in normal subjects. They believed that these negative experiments were not conclusive because changes in blood flow are not always reflected by changes in skin temperature. They pointed out that the loss of vasoconstrictor tone raised the temperature of the part to such a degree that further active vasodilatation had little chance of causing a further rise in skin temperature. Grant and Holling (3) studied the blood flow in the forearm during intensive body heating. They found that the blood flow increased, and that this increase was dependent on the integrity