title: Isoflurane depresses baroreflex control of heart rate in decerebrate rats.
abstract: BACKGROUND
  Isoflurane inhibits baroreflex control of heart rate (HR) by poorly understood mechanisms. The authors examined whether suprapontine central nervous system cardiovascular regulatory sites are required for anesthetic depression.
  
  
  METHODS
  The effects of isoflurane (1 and 2 rat minimum alveolar concentration [MAC]) on the baroreflex control of HR were determined in sham intact and midcollicular-transected decerebrate rats. Intravenous phenylephrine (0.2-12 microg/kg) and nitroprusside (1-60 microg/kg) were used to measure HR responses to peak changes in mean arterial pressure (MAP). Sigmoidal logistic curve fits to HR-MAP data assessed baroreflex sensitivity (HR/MAP), HR range, lower and upper HR plateau, and MAP at half the HR range (BP50). Four groups (two brain intact and two decerebrate) were studied before, during, and after isoflurane. To assess sympathetic and vagal contributions to HR baroreflex, beta-adrenoceptor (1 mg/kg atenolol) or muscarinic (0.5 mg/kg methyl atropine) antagonists were administered systemically.
  
  
  RESULTS
  Decerebration did not alter resting MAP and HR or baroreflex parameters. Isoflurane depressed baroreflex slope and HR range in brain-intact and decerebrate rats. In both groups, 1 MAC reduced HR range by depressing peak reflex tachycardia. Maximal reflex bradycardia during increases in blood pressure was relatively preserved. Atenolol during 1 MAC did not alter maximum reflex tachycardia. In contrast, atropine during 1 MAC fully blocked reflex bradycardia. Therefore, 1 MAC predominantly depresses sympathetic components of HR baroreflex. Isoflurane at 2 MAC depressed both HR plateaus and decreased BP50 in both groups.
  
  
  CONCLUSIONS
  Isoflurane depresses HR baroreflex control by actions that do not require suprapontine central nervous system sites. Isoflurane actions seem to inhibit HR baroreflex primarily by the sympathetic nervous system.
authors: Oregon Health & Science University, Portland, Oregon 97201, USA.
authors: Jong S
authors: JS
authors: Lee
authors: Don
authors: D
authors: Morrow
authors: Michael C
authors: MC
authors: Andresen
authors: Kyoung S K
authors: KS
authors: Chang
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000465:Algorithms; D018685:Anesthetics, Inhalation / Q000494:pharmacology*; D000818:Animals; D001262:Atenolol / Q000494:pharmacology; D001285:Atropine / Q000494:pharmacology; D017776:Autonomic Pathways / Q000187:drug effects; D017704:Baroreflex / Q000187:drug effects*; D001784:Blood Gas Analysis; D003655:Decerebrate State / Q000503:physiopathology*; D006339:Heart Rate / Q000187:drug effects*; D006400:Hematocrit; D006439:Hemodynamics / Q000187:drug effects; D007530:Isoflurane / Q000494:pharmacology*; D008297:Male; D018727:Muscarinic Antagonists / Q000494:pharmacology; D011188:Potassium / Q000097:blood; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000097:blood
chemical_list: D000319:Adrenergic beta-Antagonists; D018685:Anesthetics, Inhalation; D018727:Muscarinic Antagonists; D001262:Atenolol; D001285:Atropine; D012964:Sodium; D007530:Isoflurane; D011188:Potassium