Neurogenic control of cerebral blood flow

Abstract

In experiments on 15 isolated dog brains, cerebral blood flow could be influenced by short (20 sec) supramaximal, unilateral electrical stimulation of the vagoysympathetic trunk, the trigeminal nerve and the medulla oblongata. The changes in cerebral vascular resistance and cerebral oxygen consumption developed 2 sec after onset of the stimulation, reaching their peak 30 sec later and lasted up to 3 min. During sympathetic stimulation cerebral blood flow decreased from 47.2 ml to 42.0 ml 100 g tissue/min and cerebral vascular resistance increased about 18%. This constrictor effect was completely blocked by phentolamine. During vagal stimulation no effect could be observed. During trigeminal stimulation cerebral blood flow increased from 44.0 ml to 48.9 ml 100 g tissue/min, cerebral vascular resistance decreased about 19%, and cerebral oxygen consumption increased about 12%. Reliable inhibition of this dilating response was not achieved with either propranolol or atropine and it is assumed that there are no vasodilator fibers in the trigeminal nerve. During medullary stimulation cerebral blood flow increased from 42.0 ml to 54.7 ml 100 g tissue/min, cerebral vascular resistance decreased about 45% and cerebral oxygen consumption increased about 23%. The diminishing effects of propranolol and atropine on this dilating response was not statistically significant. A restricted region in the medulla is presented from which changes in cerebral blood flow produced by electrical stimulation were not associated with changes in the electrical pattern of the brain. Observations that the vascular and functional reactions of the brain can be dissociated point to a role of the medulla in regulating cerebral blood flow, but do not elucidate the mechanism. In general, the results support evidence that a double—metabolic and neurogenic—mechanism is involved in the control of cerebral blood flow. It is suggested that the effects during vagosympathetic stimulation are completely neurogenic, the effects during trigeminal stimulation mainly metabolic, and the effects during medullary stimulation both metabolic and neurogenic in origin.