SUMMARY1. Sympathetic nerve discharge (SND) of three postganglionic nerves with different functions and anatomical locations was simultaneously recorded at rest and during severe cerebral ischaemia (Cushing reaction). The three nerves, controlling the heart (inferior cardiac nerve), visceral (renal nerve) and skeletal muscle circulation (vertebral nerve), were selected with the assumption that their activity pattern will represent the differential central autonomic command to the major players of the circulatory response to cerebral ischaemia.2. Changes in the power density spectra of the nerve signals, and in the pairwise coherence functions, elicited by the cerebral ischaemia, were evaluated separately for the rhythmic (R-SND, i.e. between 0 and 6 Hz) and high-frequency (HF-SND, i.e. between 12 and 100 Hz) components of the nerve signals.3. The sympathetic nerve response to cerebral ischaemia developed in two phases. Phase 1 was a massive R-SND reaction and phase 2 was characterized by SND desynchronization and by the emergence of HF-SND. The power of HF-SND occupied a wide band between 12 and 80 Hz with maximum between 20 and 30 Hz. All three nerves were involved in the Cushing response but the magnitude and character of the reactions were specific for each nerve. In the cardiac nerve, the power of the rhythmic component of the discharge increased almost twice the control and remained dominant during the whole reaction, strongly modulating HF-SND during the second phase. In the vasomotor nerves, R-SND was suppressed during phase 2 and HF-SND occupied 65 % of the total power of the signal. Near equal Rto HF-SND proportions, however, were reached on different activity levels in renal and vertebral nerves. Whereas total renal SND did not change, the power of the vertebral SND increased more than twice. In addition, desynchronization in the vertebral SND was preceded by a massive R-SND reaction during phase 1, which was missing in the renal nerve.4. For all possible nerve pairs, R-SND was highly coherent before the reaction and remained so during intracranial pressure elevation, regardless of the direction and magnitude of the changes in absolute and/or relative power of this component in different nerves. On the other hand, HF-SND never correlated between any of the MS 1149 B. KOCSIS AND OTHERS nerve pairs indicating that this component in each nerve originated from specific sources of regional sympathetic activity.5. We conclude that the sympathetic nervous system is capable of generating different types of activity, including rhythmic and desynchronized discharges, and these activity patterns play an important role in generating differential sympathetic nerve response to cerebral ischaemia. Different sympathetic networks controlling different cardiovascular effectors, due to their specific properties (i.e. unequal capability of synchronization or desynchronization of the discharge), may convert the general excitatory effect of the cerebral ischaemia into specific discharge patterns with characteristic involvem...

The present study was designed to determine the extent to which the brain stem neural networks, normally capable of synchronizing the sympathetic nerve discharge (SND) into 2- to 6- and 10-Hz rhythmic fluctuations, contribute to the control of autonomic reactions during brain hypoxia and/or hypercapnia. Vertebral, cardiac, and renal nerve discharges were recorded electrophysiologically in 34 anesthetized, curarized, and artificially ventilated cats. The sympathetic nerve responses to cerebral ischemia (elicited by reducing the blood supply to the brain), intracranial pressure elevation (Cushing reaction), and systemic asphyxia were tested with special focus on the rhythmic structure of the SND. It has been found that there are two phases of SND changes during cerebral ischemia differing mainly in the frequency content of the signals and less in the compound action potential amplitude. During the first phase the rhythmic generators controlling the tonic sympathetic outflow are more strongly activated, which is reflected in a stronger, more regular, and more widespread manifestation of these rhythms on the efferent neurograms. After some time the normal SND structure abruptly changes to a desynchronized activity with loss of the three main sympathetic rhythms and responsiveness to baroreceptor reflex activation. The same stereotyped changes can be observed regardless of the way in which the brain hypoxia and/or hypercapnia has been produced. Nor does the denervation of peripheral baro- and chemoreceptors substantially alter the general pattern of the responses.

The performance of the sympathetic nervous system during sustained moderate cerebral ischemia (CI) was examined in the present study. For this purpose, a Cushing response was elicited repeatedly during incomplete global CI in anesthetized artificially ventilated cats after vagotomy and baroreceptor denervation. In control animals without CI, sympathetic activity in response to brief elevation of intracranial pressure (ICP) showed a well-repeatable two-phase reaction. During CI there was a progressive deterioration of background sympathetic nerve discharge (SND) over a period of 30 min. SND response to repeated elevation of ICP was initially similar to control response but later with progression of CI was seriously changed. 1) Instead of the usual hyperactivation, sympathetic nerve activity was depressed during intracranial hypertension. 2) The characteristic desynchronized activity either appeared later during the reperfusion period or remained absent. The progressive loss of SND response to raised ICP in developed CI was compared with the changes seen in experiments in which repeated ICP elevations were superimposed on asphyxia. These findings suggest that the sympathetic component of the Cushing reaction strongly depends on the actual state of brain stem autonomic circuits and may be seriously altered in pathological situations involving ischemic brain injury.

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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.