title: Differential sympathetic reactions during cerebral ischaemia in cats: the role of desynchronized nerve discharge.
abstract: 1. 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 R- to 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 nerve pairs indicating that this component in each nerve originated from specific sources of regional sympathetic activity.(ABSTRACT TRUNCATED AT 400 WORDS)
authors.affiliation: Department of Physiology, National Institute of Neurosurgery, Budapest, Hungary.
authors.forename: B
authors.initials: B
authors.lastname: Kocsis
authors.forename: L
authors.initials: L
authors.lastname: Fedina
authors.forename: K
authors.initials: K
authors.lastname: Gyimesi-Pelczer
authors.forename: T
authors.initials: T
authors.lastname: Ladocsi
authors.forename: E
authors.initials: E
authors.lastname: Pasztor
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002545:Brain Ischemia / Q000503:physiopathology*; D002415:Cats; D006321:Heart / Q000294:innervation / Q000503:physiopathology; D007427:Intracranial Pressure / Q000502:physiology; D007668:Kidney / Q000294:innervation / Q000503:physiopathology; D009132:Muscles / Q000294:innervation / Q000503:physiopathology; D009474:Neurons / Q000502:physiology; D013564:Sympathetic Nervous System / Q000503:physiopathology*