Thyrotropin-releasing hormone (TRH) causes sympathetic activation and cerebral vasodilation in the rabbit.

The effects of TRH on regional blood flow were studied in rabbits under urethane anesthesia. Four types of experiments were performed with the following results. (1) I.v. injection of 2 mg/kg b.w. TRH in animals with unilateral cervical sympathotomy caused a rise in mean arterial blood pressure from 10.0 +/- 0.5 to 13.3 +/- 0.5 kPa. Total cerebral blood flow, measured with labeled microspheres, increased from 75 +/- 5 to 126 +/- 16 g/min/100 g tissue on the intact side. There was a similar increase on the side with sympathotomy. The greatest increase, about 70%, was observed in cortical gray matter, caudate nucleus and thalamic region. There were marked reductions in blood flows in the spleen, gastric mucosa, skin and skeletal muscle. Mydriasis occurred on the side with an intact sympathetic supply. (2) I.v. infusion of 0.06 mg/kg b.w. per min TRH in animals with unilateral cervical sympathotomy and stabilized blood pressure increased total cerebral blood flow from 84 +/- 10 to 139 +/- 7 g/min/100 g. Blood flows to the masseter muscle, submandibular gland and facial skin but not to the eye or tongue were markedly reduced on the side with an intact sympathetic supply while little or no effect was observed on the side with sympathotomy. (3) Unilateral peripheral stimulation of the sympathetic chain at 1 Hz after bilateral sympathotomy caused a reduction in blood flows in the tongue, masseter muscle, submandibular gland and facial skin in animals with stabilized blood pressure. No potentiation of the stimulation effect was observed during TRH infusion. (4) The arteriovenous difference in oxygen saturation in the brain decreased from 39.1 +/- 2.8 to 26.4 +/- 3.7% after i.v. injection of 2 mg/kg b.w. TRH. The results indicate that TRH caused cerebral vasodilation in excess of that required by possible changes in cerebral metabolism. The vasoconstriction in the head region and the mydriasis was caused mainly by an increase in the activity of the cervical sympathetic nerves.