Abstract
In curarized cats narcotized with amytal or pentobarbital, a small artificially cooled thermocouple introduced directly into the hypothalamic tissue yielded no evidence of vasodilator innervation. Vasoconstriction was quite regularly produced by stimulation of the cervical sympathetic; the effect was slow in onset, progressed after stimulation, and usually was irreversible and not re-peatable. Corresponding observations made in the tem-poral muscle and tongue indicate that these characteristics belong to the hypothalamic vessels and not to the recording instrument or nerve excitation employed. A humoral mechanism is suggested. CO2-excess, O2-lack, and asphyxia dilated the hypothalamic vessels; CO2-decrease (increased ventilation) constricted them. O2 occasionally constricted them slightly, but changes in pH produced by fixed acid or alkali had no direct effect. COa appeared to have a specific dilator influence here as well as in the medulla. Adrenalin frequently caused relatively weak but rather prolonged constriction of hypothalamic vessels. Pituitrin and Ca had no direct effect. Histamine and a choline derivative were active dilators. The effects of adrenalin, histamine, and choline derivatives were definitely less marked in the hypothala-mus than in the temporal muscle or tongue, so that a selective action by any of these agents on the hypothalamic circulation is improbable. At present it appears that the vasoconstriction produced in the hypo-thalamus by cervical sympathetic stimulation has no great physiologic significance since it can be elicited only by a highly artificial stimulus. Attempts at detecting an intrinsic vasoconstrictor mechanism were unsuccessful. An intrinsic chemical regulation, with CO2 playing the dominant part, seems more important than nerve control.

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