title: The effect of sevoflurane on spontaneous sympathetic activity, A delta and C somatosympathetic reflexes, and associated hemodynamic changes in dogs.
abstract: This study examined the effect of sevoflurane on spontaneous renal sympathetic nerve activity (RSNA), A delta- and C-fiber-mediated somatosympathetic reflexes, and hemodynamic changes in anesthetized dogs. RSNA, and A delta and C reflexes evoked by electrical stimulation of the radial nerve were observed in multifiber recordings of efferent activity in renal sympathetic nerves. Sevoflurane was administered at 1%, 2%, 3%, and 4% end-tidal concentrations for periods of 20 min. The mean A delta reflexes decreased by 20%, 39%, and 54% (P < 0.05 to < 0.01), and the C reflexes decreased by 38%, 62%, and 74% (P < 0.05 to < 0.01) at concentrations of 2%, 3%, and 4%, respectively. The relatively greater effect on C reflexes was significant (P < 0.05) and comparable with the effect of mu-opioids. There was no change in mean RSNA, heart rate (HR), and cardiac output (CO) up to 3% sevoflurane, but these decreased by 36%, 24%, and 13% (P < 0.05), respectively, at 4% sevoflurane. Sevoflurane 1%-4% caused a virtually linear reduction in systemic vascular resistance (SVR) from 7% (P < 0.05) to 44% (P < 0.05), together with a reduction in mean arterial pressure (MAP) that was significant for concentrations greater than 2%. The results indicate that sevoflurane causes a greater depression of C compared with A delta reflexes, and that the reduction in MAP was entirely due to a decrease in SVR up to 3%, whereas at 4% sevoflurane, reductions in sympathetic activity, HR, and CO also contributed its depressor effect.
  
  
  CONCLUSIONS
  The relatively greater depressant effect of sevoflurane on C compared with A delta nociceptive somatosympathetic reflexes is similar to mu-opioids. The hypotensive effect of sevoflurane was significant at 2% concentration, whereas heart rate, cardiac output and sympathetic activity were reduced only at concentrations greater than 3%.
authors.affiliation: Department of Anaesthetics and Intensive Care, Imperial College School of Medicine, Hammersmith Hospital, London, England. d.ma@rpms.ac.uk
authors.forename: D
authors.initials: D
authors.lastname: Ma
authors.forename: C
authors.initials: C
authors.lastname: Wang
authors.forename: C K
authors.initials: CK
authors.lastname: Pac Soo
authors.forename: M K
authors.initials: MK
authors.lastname: Chakrabarti
authors.forename: G G
authors.initials: GG
authors.lastname: Lockwood
authors.forename: J G
authors.initials: JG
authors.lastname: Whitwam
mesh_terms: D018685:Anesthetics, Inhalation / Q000494:pharmacology*; D000818:Animals; D004285:Dogs; D005260:Female; D006439:Hemodynamics / Q000187:drug effects*; D008297:Male; D008738:Methyl Ethers / Q000494:pharmacology*; D009412:Nerve Fibers / Q000187:drug effects* / Q000502:physiology; D009413:Nerve Fibers, Myelinated / Q000187:drug effects* / Q000502:physiology; D011311:Pressoreceptors / Q000187:drug effects / Q000502:physiology; D012018:Reflex / Q000187:drug effects*; D000077149:Sevoflurane; D013564:Sympathetic Nervous System / Q000187:drug effects*
chemical_list: D018685:Anesthetics, Inhalation; D008738:Methyl Ethers; D000077149:Sevoflurane