Owing to the large amount of conflicting data regarding the activity of the pulmonary vasomotor nerves, modern reviewers of the literature generally conclude that vasomotor influences play no important part in the regulation of the pulmonary blood flow. Previous work on the subject falls sharply into two groups, experiments on the whole animal and those on isolated perfused lungs. It must be confessed that a careful survey of the work on the whole animal purporting to demonstrate the functional activity of these nerves reveals with few exceptions the absence of a sufficient proof owing to the difficulties of obtaining well controlled experimental conditions, and this no doubt accounts for the scepticism prevalent at the present time. Among the doubt accounts for the scepticism prevalent at the present time. Among the exceptions are the classical experiments of Bradford and Dean (1889,
a
, 1889,
b
, 1894) on the dog, curarised and atropinised. These investigators showed that stimulation of the peripheral ends of the cut thoracic nerves from D2-D7 would sometimes cause a pulmonary arterial pressure rise without either cardiac acceleration or a systemic arterial pressure rise, and in general their results were confirmed by Francois-Franck (1895,
a
, 1895,
b
) and Plumier (1904,
a
). Excitaion of the vagus in these experiments produced no effect on the pulmonary arterial pressure, probably because, as suggested by Luck-hardt and Carlson (1921), atropine was injected to eliminate the effect of vagus stimulation on the heart. Further, they presented evidence of reflex of pulmonary vasoconstriction caused by excitation of the upper thoracic posterior roots, and Francois-Franck (1896) was able to demonstrate the same effect by stimulation of the central ends of the splachnic or anterior crural nerves. Bradford and Dean (
loc
.
Cit
.) and Weber (1910) also observed that a reflex change in the pulmonary arterial pressures occurred after central stimulation of the divided vagus nerve, and Schafer (1920) reported a reflex pulmonary arterial pressure fall after stimulation of the depressor nerve. The investigations of Bradford and Dean and of Wood (1902, 1910, 1911) on the relations of the pulmonary and aortic pressure during asphyxia were adduced as evidence in favour of the presence of a vasoconstriction nerve supply to the lungs, but the production of an adrenalinæmia in these experiments was not considered.
Serotonergic Neuron Stimulation Modulates Thalamocortical Glucose Use in the Conscious Rat
