title: Sympathetic regulation in rabbits with heart failure: experience using power spectral analysis of heart rate variability.
abstract: 1. In five intact rabbits beta-adrenoreceptor blockade (i.v. propranolol), and combined cardiac blockade (i.v. propranolol plus i.v. methscopolamine sulphate) revealed that spectral power of heart rate (HR) variability at low frequencies (LF:0.0625-0.1875 Hz) was modulated predominantly by the sympathetic nervous system and power at high frequencies (HF:0.4373-0.5625 Hz) by vagal influences. 2. In 16 rabbits resting power of HR at LF and changes in LF power in response to maximal treadmill exercise were examined prior to and after 4 and 6 weeks of doxorubicin treatment (1 mg/kg twice weekly). 3. The development of doxorubicin-induced congestive heart failure (CHF) was accompanied by a progressive increase in resting LF power [control, 8.5 +/- 2.1; 4 weeks, 13.4 +/- 1.8; 6 weeks, 21.9 +/- 3.5 (beats/min)2, P < 0.005]. 4. Power spectral analysis (PSA) of HR variability in the immediate post-exercise period showed no change from resting values in normal rabbits [5.3 +/- 1.4 vs 8.5 +/- 2.1 (beats/min)2, P > 0.05] whereas CHF rabbits showed falls in LF power after 4 weeks [4.6 +/- 1.0 vs 13.4 +/- 1.8 (beats/min)2, P < 0.005] and 6 weeks [6.5 +/- 2.4 vs 21.9 +/- 3.5 (beats/min)2, P < 0.005] of doxorubicin treatment. 5. It was concluded that PSA of HR variability reflects the autonomic regulation of sinus node function in conscious rabbits. In doxorubicin-treated animals, the rise in LF power reflects increased sympathetic activity as CHF develops. However, the apparent paradoxical fall in LF power with exercise in these animals underscores the need for caution in interpretation of PSA profiles.
authors.affiliation: Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia.
authors.forename: V
authors.initials: V
authors.lastname: Moguilevski
authors.forename: J
authors.initials: J
authors.lastname: Oliver
authors.forename: B P
authors.initials: BP
authors.lastname: McGrath
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D004195:Disease Models, Animal; D004317:Doxorubicin / Q000633:toxicity; D005080:Exercise Test; D006333:Heart Failure / Q000139:chemically induced / Q000503:physiopathology*; D006339:Heart Rate / Q000187:drug effects* / Q000502:physiology; D019832:N-Methylscopolamine; D010276:Parasympatholytics / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D011433:Propranolol / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use; D011817:Rabbits; D012602:Scopolamine Derivatives / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use; D013565:Sympatholytics / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use
chemical_list: D000319:Adrenergic beta-Antagonists; D010276:Parasympatholytics; D012602:Scopolamine Derivatives; D013565:Sympatholytics; D004317:Doxorubicin; D011433:Propranolol; D019832:N-Methylscopolamine