Hyperperfusion of the rat brain during reflex hypertension induced by sudden lowering of the cutaneous temperature

In anesthetized and artificially ventilated rats, passive or reflex hypertension was produced by ligation of the abdominal aorta (12 rats), or sudden lowering of the cutaneous temperature to 25-30 degrees C achieved by exposure to cold water (26 rats), respectively. Cold exposure increased the blood flow (microsphere method) in all of the brain regions studied by 54-174% in the face of a reflex increment in the arterial pressure by 40% on average. The vascular resistance was changed by 0-(-)32%. Such hemodynamic alterations were greater in almost all of the brain regions than would be anticipated from the autoregulatory function of the brain circulation, as evidenced by a comparison with those observed during passive hypertension. Exposure to thermoneutral water resulted in the minimal changes in the hemodynamic states of the systemic as well as brain circulations (5 rats). The sympathetic nerves innervating the cranial vessels were strongly activated during the cold exposure, as confirmed by the observation of a large increase in flow in the temporalis muscle after acute surgical sympathectomy. However, sympathetic denervation did not alter the degree of hemodynamic changes occurring in the brain regions during cold exposure. We conclude that, in the face of reflex hypertension induced by cold exposure, the powerfully activated sympathetic nerves failed to exert their well-known effect on the brain blood flow which prevents it from rising to an excessively high level.