During the 1950s and early 1960s a variety of experiments were conducted, expanding on these original observations. Many of these studies were conducted by
Professor Barcroft's protégés (Roddie, 1977; Roddie & Shepherd, 1998). In these studies (Fig. 3), conducted before rigorous human studies review boards, severe
mental or emotional stress evoked physiological changes similar to the 'defence reaction' and caused forearm blood flow to rise by up to 10-fold (for a discussion
of the mental stress used see Roddie, 1977). The forearm vasodilatation was absent after surgical sympathectomy, and in most subjects a portion of the
vasodilatation could be blunted by atropine (Fig. 3).
Along these lines, recent observations in animals indicate that chronic sympathectomy eliminates endothelial NO synthase expression
in sympathectomised blood vessels (Aliev et al. 1996). This suggests that normal NO-mediated responses to local and circulating factors would be present
following acute sympathectomy with local anaesthetics or drugs injected into the brachial artery, but that these responses would be absent in the months and
years following surgical sympathectomy.
Individual records from two subjects during periods of severe mental stress. A, in a patient with a unilateral cervical sympathectomy, mental stress
(hatched bar) evoked profound increases in forearm blood flow in the normal arm. These increases in forearm blood flow were absent in the sympathectomised forearm. B, a second subject was studied with normal innervation to both upper extremities. Atropine given selectively to one
forearm blunted but did not eliminate the vasodilator responses to severe mental stress. Adapted from Blair et al. (1959).
http://jp.physoc.org/cgi/content/full/526/3/471
