Sympathetic Activity and Plateau Waves: Experiment in Cats

Abstract

The nature of plateau waves is still unclear. In this experimental study, a possible relationship between the development of plateau waves and the activity of sympathetic vasomotor nerves was investigated using an experimental model of plateau waves produced in cats. Efferent discharge from the renal nerve activity (RNA) was recorded as an indicator for the sympathetic vasomotor tone. Intracranial pressure (ICP), systemic blood pressure (BP), endtidal CO2, cerebral blood flow (CBF), arterial blood gases, electroencephalograms (EEG) and somatosensory evoked potentials were monitored. Effects of hyperventilation and intravenous injection of mannitol on plateau waves were also studied. Experimental obstructive hydrocephalus was produced by injecting kaolin (250 mg of hydrated aluminum silicate) into the cisterna magna. Four weeks after the injection of kaolin, the central canal of the lumbar spinal cord was obliterated with a ligature placed around the dura mater. After the ligation of the spinal cord, ICP gradually increased, reaching a level of 30-100 mmHg during a period of 2-14 hours. Then, a plateau wave, a spontaneous abrupt rise in ICP up to the level of 70-160 mmHg with a duration of 4-33 minutes, was observed in all five animals. A decrease in RNA as well as in BP was observed corresponding to a rise in ICP at the initial phase of plateau waves. CBF, amplitude of EEG and somatosensory evoked potentials decreased at the peak of the plateau waves. There were no significant changes in endtidal CO2 and arterial pCO2. Plateau waves disappeared rapidly either by hyperventilation or mannitol administration. It was concluded that a temporary decrease in the sympathetic vasomotor tone in situations of increased intracranial pressure may initiate the development of plateau waves and metabolic factors secondary to brain ischemia may play a role in their perpetuation.