摘要
There is reason to believe that the vagus nerve carries sensory afferent messages from the intracranial cavity as it does from the other body cavities. Considering the arachnoid granulations as a secretory apparatus instead of an organ transporting cerebrospinal fluid, a simple model can be built. Assuming that the arachnoid granulations produce nitric oxide in accordance with changes in the intracranial pressure, the jugular foramen with the vagus nerve lying just subendothelially is where this message would be received. Other chemical substances from the granulations or other intracranial tissues could of course also act as messengers. This would mean that the brain stem could adjust to changes in intracranial pressure with small changes in cerebral venous resistance. The general idea is that intracranial pressure is a passive function of the intracranial pressure-volume relationship. But the hypothesis suggests that the vagus nerve constantly mediates changes in intracranial pressure to the brain stem that can rapidly adjust cerebral venous resistance. This control is totally intracranial and easily overridden by considerable changes in absorption of spinal fluid or intracranial calamities. This article looks for clues in support of the idea that the vagus nerve mediates intracranial pressure changes to the brain stem.
There is reason to believe that the vagus nerve carries sensory afferent messages from the intracranial cavity as it does from the other body cavities. Considering the arachnoid granulations as a secretory apparatus instead of an organ transporting cerebrospinal fluid, a simple model can be built. Assuming that the arachnoid granulations produce nitric oxide in accordance with changes in the intracranial pressure, the jugular foramen with the vagus nerve lying just subendothelially is where this message would be received. Other chemical substances from the granulations or other intracranial tissues could of course also act as messengers. This would mean that the brain stem could adjust to changes in intracranial pressure with small changes in cerebral venous resistance. The general idea is that intracranial pressure is a passive function of the intracranial pressure-volume relationship. But the hypothesis suggests that the vagus nerve constantly mediates changes in intracranial pressure to the brain stem that can rapidly adjust cerebral venous resistance. This control is totally intracranial and easily overridden by considerable changes in absorption of spinal fluid or intracranial calamities. This article looks for clues in support of the idea that the vagus nerve mediates intracranial pressure changes to the brain stem.
