Activity of peripheral sympathetic efferent nerves in experimental subarachnoid haemorrhage. Part I: Observations at the time of intracranial hypertension.

The origin and pathomechanism of vegetative disturbances in patients suffering from subarachnoid haemorrhage are not completely clarified. Since some of these alterations in vegetative functions may well be attributed to acute changes in sympathetic activity, we initiated a study to investigate this modality in experimentally induced subarachnoid haemorrhage. Experiments were performed on 51 cats, anaesthetized with alpha-chloralose and urethane, immobilized and artificially ventilated. Compound electrical discharges of the left vertebral, cardiac and renal sympathetic nerves, ECG, EEG, end-tidal CO2, systemic arterial blood pressure and intracranial pressure were recorded on a polygraph. Subarachnoid haemorrhage was simulated by the injection of 1-5 ml of fresh, autologous blood into the cisterna magna. Mock cerebrospinal fluid was also injected as a control. Our results showed that in induced subarachnoid haemorrhage, not the blood itself but the intracranial pressure elevation might be responsible for the strong increase in sympathetic efferent activity. With the direct recording of the electrical activity of the three sympathetic nerves, we were able to verify the sympathetic overactivity underlying the cardiovascular disturbances during intracranial pressure elevation. Regarding the mechanism of the overactivity, most probably not the ischaemia or hypoxia, but the mechanical distortion of the medulla could be the adequate stimulus of the sympathetic overactivity and the Cushing response during intracranial pressure elevation.