Arterial Baroreflex Control of the Sinus Node During Dobutamine Exercise Stress Testing

Abstract

Abstract-The contributions of increases in circulating catecholamines, changes in central command, and muscle afferents on baroreflex control of the sinus node during exercise are unclear. We used a dobutamine infusion to induce hemodynamic changes comparable to those of moderate physical exercise in the absence of changes in central command and muscle afferents in 13 healthy subjects. Dobutamine (up to 9 g/kg body weight per minute) increased systolic blood pressure, shortened the RR interval, increased systolic blood pressure variability, but blunted RR interval variability (PϽ0.05 versus placebo). Consequently, dobutamine decreased the coherence between variations in systolic blood pressure and RR interval and decreased arterial baroreflex sensitivity from 12Ϯ2 to 3Ϯ1 ms/mm Hg (PϽ0.01). The largest increases in systolic blood pressure with dobutamine were paralleled by the greatest impairments in arterial baroreflex sensitivity (0.50ϽrϽ0.56, PϽ0.01). The chronotropic effects of dobutamine prevented a reflex bradycardia in response to the blood pressure increase. However, less predominant low-frequency oscillations in systolic blood pressure (PϽ0.0001) suggested preserved sympathetic withdrawal in response to the blood pressure increase induced by dobutamine. In conclusion, this study revealed that a shift in the operating point of the arterial baroreceptors and the chronotropic effects of adrenergic stimulation impair baroreflex control of the sinus node during dobutamine exercise stress testing. Baroreflex control of the sinus node is not reset when hemodynamic characteristics of exercise are reproduced in the absence of modifications in central command and muscles afferents. (Hypertension. 1999;33:987-991.)

Postoperative goal-directed therapy and development of acute kidney injury following major elective noncardiac surgery: post-hoc analysis of POM-O randomized controlled trial

“…We have previously reported that GDT in the same trial is associated with reduced cardiac (vagal) parasympathetic activity, as revealed by changes in heart rate variability and despite similar heart rates between groups [13]. A similar observation in reduced cardiac (vagal) parasympathetic activity has been described during stress echocardiography [36, 37]. Furthermore, we have also shown in separate cohorts of patients that impaired baroreflex dysfunction—which is in part characterized by reduced parasympathetic tone—is also associated with excess morbidity [38, 39].…”

Peripheral sympathetic control during dobutamine infusion

“…These findings contrast with our study where large and sustained hemodynamic improvements with dobutamine did not modify the markedly elevated sympathetic activity in patients with severe CHF. Dobutamine does not improve baroreflex sensitivity (19,31). Our study, therefore, emphasizes the importance of arterial baroreflex activation on sympathetic nerve inhibition during pharmacologic interventions that do not improve arterial baroreflex function (19,22,(31)(32)(33).…”

“…Dobutamine does not improve baroreflex sensitivity (19,31). Our study, therefore, emphasizes the importance of arterial baroreflex activation on sympathetic nerve inhibition during pharmacologic interventions that do not improve arterial baroreflex function (19,22,(31)(32)(33). Limited hemodynamic improvements during short-term dobutamine infusion did not improve sympathetic activity in CHF patients (20).…”

Dobutamine “Stress” Test and Latent Cardiac Susceptibility to Inhaled Diesel Exhaust in Normal and Hypertensive Rats

“…Dobutamine is known to increase HR and BP artificially and also to blunt baroreceptor function (van de Borne et al 1999; Zaza and Lombardi 2001), which normally would elicit a vagal reflex when BP increases. Van de Borne et al (1999) found that the largest decreases in baroreflex sensitivity (BRS) occurred during the largest increases in BP induced by dobutamine.…”