頭蓋内圧亢進およびクモ膜下出血時における交感神経系の反応について

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The direct observation of the sympathetic vasomotor activity during increase in intracranial pressure (ICP) has seldom been done, although the pressor response following increased ICP is presumed to be due to excitation of the sympathetic nervous system. It is also interesting to know whether the sympathetic nervous system participates in the development of vasoparalysis or plateau wave. The activity of the sympathetic vasomotor nerve was assessed by measuring the efferent discharge from the renal nerve of a cat which is known to be a good indicator for evaluating the sympathetic vasoconstrictor tone of the whole body. ICP was increased stepwisely by infusing saline into the cistena magna. With each increment of ICP, the renal nerve activity (RNA) was suppressed. Since the suppression of the RNA was not striking in the animals whose baroreceptor nerves had been cut, it is convinced that a reflex mechanism via the baroreceptor depresses the sympathetic vasoconstrictor tone during the initial phase of increased ICP. At cerebral perfusion pressure (CPP) of 30 mmHg, a sudden remarkable increase of the RNA was noted, followed by a significant rise of blood pressure (BP) When increased ICP was lowered, the RNA was decreased to the level below the initial value After the procedure of raising and lowering ICP was repeated, in one cat out of five, an abrupt disappearance of RNA for five minutes was observed during the state of increased ICP. The renal nerve did not respond to the withdrawal of blood, which usually causes the RNA to increase. The sympathetic vasomotor activity was considered to be paralyzed temporarily during this phase. In other animals whose ICP were raised by infusing heparinized arterial blood instead of normal saline, the increase in RNA from the suppressed state occurred at earlier stage, that is, at higher level of CPP. In one cat out of five, the infusion of a small amount of blood caused a remarkable continous increase in RNA followed by a significant rise in BP with tachycardia. These observations indicate the tone of the sympathetic nervous system may be increased in subarachnoid hemorrhage. In other five animals, ICP was elevated rapidly beyond the level of mean BP and maintained for seven minutes and then lowered. After this procedure was repeated several times, in three cats out of these five, a gradual decline of RNA was observed following the stage of increase resulted from the elevation of ICP. Thereafter, RNA disappeared completely despite ICP maintained above the level of BP. The absence of RNA persisted several minutes even after the ICP was lowered. The administration of 0.025mg/kg of norepinephrine at this stage resulted in a significant rise in ICP following a rise in BP. Several minutes later, RNA was recovered spontaneously to the level more than that before the procedure. The administration of norepinephrine at this stage of increased RNA resulted in only a slight rise in ICP, while the rise in BP was similar. This phenomenon may strongly suggest the possibility that the tone of the sympathetic vasoconstrictor nerve plays an important role for protecting the brain against the change in BP by preventing the occurrence of sudden rise in ICP.
日本脳神経外科学会の論文

頭蓋内圧亢進およびクモ膜下出血時における交感神経系の反応について

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