This study tested the hypothesis that abnormalities of baroreceptor-mediated suppression of sympathetic activity may persist in chronic congestive heart failure (CHF) despite pharmacologic treatment and clinical stability. Plasma norepinephrine and norepinephrine kinetics (using 3HNE infusions) were measured during head-up and head-down tilt in 8 patients with chronic CHF and 6 normal control subjects. In response to upright tilt, normal subjects increased plasma norepinephrine (270 ± 45 to 413 ± 60 pg/ml, p < 0.001) and norepinephrine spillover (540 ± 103 to 781 ± 124 ng/min, p < 0.001). Patients also increased plasma norepinephrine (436 ± 105 to 600 ± 112 pg/ml, p < 0.05) and norepinephrine spillover (802 ± 180 to 1,037 ± 370 ng/min). During head-down tilt, plasma norepinephrine decreased in normal subjects (from 413 ± 60 to 256 ± 26 pg/ml, p < 0.001). The decrease was due entirely to a decrease in norepinephrine spillover (781 ± 124 to 466 ± 40 ng/min, p < 0.001). In contrast, there was no significant change in norepinephrine spillover (1,037 ± 370 to 949 ± 338 ng/min) during head-down tilt in patients with CHF. These data suggest that suppression of sympathetic activity during baroreceptor loading may be defective in CHF despite relative preservation or correction of the response to baroreceptor unloading.
Bibliographical noteFunding Information:
From the Hennepin County Medical Center and the University of Minnesota, Minneapolis, Minnesota. This research was supported by a Grant-in-Aid from the American Heart Association, Dallas, Texas, and by Program Project Grant POlHL32427 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland. Dr. Goldsmith is an Established Investigator of the American Heart Association and Ciba-Geigy Corporation. Manuscript received August $1991; revised manuscript received and accepted November 12, 199 1.