Does respiratory sinus arrhythmia serve a buffering role for diastolic pressure fluctuations?
Though many consider the magnitude of respiratory sinus arrhythmia as an index of cardiac vagal control, its physiological origins remain unclear. One influential model postulates that the systolic pressure rise within a given beat stimulates the baroreflex arc to adjust the following heart period such that diastolic pressure is "stabilized" and hence displays lesser fluctuation. Accordingly, the magnitude of diastolic pressure fluctuations with respiration should change reciprocally after augmentation or inhibition of respiratory sinus arrhythmia. To test this, we augmented and subsequently inhibited respiratory sinus arrhythmia with vagotonic and vagolytic atropine administration in 19 healthy young volunteers to assess the relation between respiratory R-R interval and diastolic pressure fluctuations. Respiratory diastolic pressure fluctuations showed parallel rather than inverse changes in relation to those in respiratory sinus arrhythmia: they increased with augmented respiratory sinus arrhythmia (138 and 190% of baseline in the frequency and time domains, both P < 0.05) and tended to decrease with inhibited respiratory sinus arrhythmia (82 and 93% of baseline in frequency and time domains, P = 0.20 and P = 0.07). Furthermore, >60% of the change in diastolic pressure fluctuations was explained by the change in respiratory sinus arrhythmia (R(2) = 0.62; P < 0.001), that is, an approximately 50-ms increase or decrease in respiratory sinus arrhythmia resulted in a parallel approximately 1-mmHg change in diastolic pressure fluctuations. Thus, in young healthy individuals during supine rest, respiratory fluctuations in R-R interval do not buffer against diastolic pressure fluctuations but actually cause diastolic pressure fluctuations. Therefore, our data provide little evidence for a predominant role of a baroreflex feedback mechanism underlying respiratory sinus arrhythmia during supine rest.
Tan
Can Ozan
CO
Cardiovascular Research Laboratory, Spaulding Rehabilitation Hospital, 125 Nashua Street, Boston, MA 02114, USA. cotan@partners.org
Taylor
J Andrew
JA
D000328:Adult; D000818:Animals; D001146:Arrhythmia, Sinus / Q000503:physiopathology*; D001285:Atropine / Q000494:pharmacology; D017704:Baroreflex / Q000187:drug effects / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D003627:Data Interpretation, Statistical; D003971:Diastole / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D008297:Male; D018727:Muscarinic Antagonists / Q000494:pharmacology; D012044:Regression Analysis; D015656:Respiratory Mechanics / Q000502:physiology*; D014630:Vagus Nerve / Q000187:drug effects / Q000502:physiology; D055815:Young Adult
D018727:Muscarinic Antagonists; D001285:Atropine