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William F. Collins, James L. O'Leary, William E. Hunt and Henry G. Schwartz

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William E. Hunt, Bertha A. Bouroncle and John N. Meagher

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William E. Hunt, John N. Meagher and James E. Barnes

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William E. Hunt, J. N. Meagher, A. Friemanis and C. W. Rossel

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The Carpal-Tunnel Syndrome

Diagnosis and Treatment

William E. Hunt and William T. Luckey

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William E. Hunt and Robert M. Hess

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Intramural neural elements in components of the carotid bifurcation

A histological basis for differential function

Sheldon B. Meyerson, James L. Hall and William E. Hunt

✓ The histology of the specialized region of the carotid bifurcation in man was studied with Orcein stain for elastic tissue, Masson's trichrome for muscle and connective tissue, and Bodian's silver method for neural elements. Four distinct regions exist: the common carotid, which appears to be solely a conduit; the carotid sinus, which is thin and very elastic with its baroreceptors in the medial wall; the external carotid, which is highly muscular and presumably active; and the internal carotid, also highly muscular and presumably active. The transition between zones is abrupt. Prominent clusters of up to 30 or 40 multipolar nerve cells, 15 to 25 µ in diameter, were found in the subintimal region of the internal carotid artery, some in the common, and a few in the external carotid. Occasional rounder cells of similar size with only one process were seen, possibly of sensory type. No cell bodies were seen in the adventitia of any vessel. No relation to the perivascular plexus was established. It is speculated that the neurons may be related to the reported local differential response to environment by the internal and external carotid systems.

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David Yashon, George E. Locke, W. George Bingham Jr., Wigbert C. Wiederholt and William E. Hunt

✓ Electrocortigraphic activity and common carotid blood flow were studied in 12 dogs during and following profound oligemic hypotension. Five animals survived but seven died within 75 min of hypotension. Although an 80% to 90% reduction in both mean arterial pressure and common carotid blood flow was observed, only a 20% diminution of intracranial pressure occurred and there was little change in electrocorticographic function. The preservation of cerebral function in the presence of profound systemic hypotension was demonstrated. When death occurred during shock, no prior change in central nervous system function was noted. With reinfusion, no change in parameters was noted, but common carotid blood flow was depressed to 35% to 50% of control levels for up to 2½ hrs of observation.