抄録
The sympathetic regulation of heart rate (HR) may be attained by neural and humoral factors. With respect to the humoral factor, plasma noradrenaline (NA) and adrenaline (Adr) can reportedly increase to levels approximately 10 times higher than resting level during severe exercise. Whether such high plasma NA or Adr interfered with the sympathetic neural regulation of HR remained unknown. We estimated the transfer function from cardiac sympathetic nerve stimulation (SNS) to HR in anesthetized and vagotomized rabbits. An intravenous administration of NA (n = 6) at 1 and 10 μg·kg−1·h−1 increased plasma NA concentration (pg/ml) from a baseline level of 438 ± 117 (mean ± SE) to 974 ± 106 and 6,830 ± 917 (P < 0.01), respectively. The dynamic gain (bpm/Hz) of the transfer function did not change significantly (from 7.6 ± 1.2 to 7.5 ± 1.1 and 8.1 ± 1.1), whereas mean HR (in bpm) during SNS slightly increased from 280 ± 24 to 289 ± 22 (P < 0.01) and 288 ± 22 (P < 0.01). The intravenous administration of Adr (n = 6) at 1 and 10 μg·kg−1·h−1 increased plasma Adr concentration (pg/ml) from a baseline level of 257 ± 86 to 659 ± 172 and 2,760 ± 590 (P < 0.01), respectively. Neither the dynamic gain (from 8.0 ± 0.6 to 8.4 ± 0.8 and 8.2 ± 1.0) nor the mean HR during SNS (from 274 ± 13 to 275 ± 13 and 274 ± 13) changed significantly. In contrast, the intravenous administration of isoproterenol (n = 6) at 10 μg·kg−1·h−1 significantly increased mean HR during SNS (from 278 ± 11 to 293 ± 9, P < 0.01) and blunted the transfer gain value at 0.0078 Hz (from 5.9 ± 1.0 to 1.0 ± 0.4, P < 0.01). In conclusion, high plasma NA or Adr hardly affected the dynamic sympathetic neural regulation of HR.
