No abstract

Peroneal muscle sympathetic nerve activity (MSA), finger blood pressure and cardiac intervals were recorded at rest in 60 healthy subjects, aged 18–71 years. Arterial baroreflex control of MSA was analysed by relating each spontaneous sympathetic burst to the diastolic blood pressure and the cardiac interval of the heart beat during which the burst was generated. The results were expressed as blood pressure/cardiac interval threshold for occurrence of bursts, and as baroreflex sensitivity (i.e. the relationship between diastolic pressure/cardiac interval and burst strength). Significant blood pressure/cardiac interval thresholds were present in all subjects and old subjects had less variability of thresholds than young subjects. In contrast, significant baroreflex sensitivity for diastolic pressure and cardiac interval was present in only 55 and 73 % of the subjects, respectively. There was no age‐related difference in sensitivity. In 40 subjects, two 5 min periods from the same recording were analysed. The number of sympathetic bursts and the threshold for occurrence of bursts were reproducible in all subjects. In contrast, significant baroreflex sensitivity in both periods was present in only 30 % (diastolic pressure) and 40 % (cardiac interval) of the subjects. The results show that the baroreflex mechanisms regulating the occurrence and strength of sympathetic bursts are not identical. We suggest that the modulation occurs at two sites, one which determines whether or not a burst will occur, and another at which the strength of the discharge is determined.

No abstract

No abstract

These results indicate a selective increase in cardiac adrenergic drive (increased amounts of transmitter available at neuroeffector junctions) in patients with mild-to-moderate CHF. This increase appears to precede the augmented sympathetic outflow to the kidneys and skeletal muscle found in advanced CHF.

No abstract

Muscle sympathetic activity (MSA) was recorded in the peroneal nerve during sleep in 14 sleep-deprived healthy subjects. Continuous noninvasive recordings of finger blood pressure were obtained in 7 subjects. In light sleep (stage 2 sleep) the number of sympathetic bursts/min decreased to 90 +/- 8% (mean +/- SEM) and total MSA (= burst/min x mean burst area) to 89 +/- 5% of the awake value (P less than 0.05, n = 14). In deep sleep (stage 3-4) total MSA decreased further, to 71 +/- 8% of the awake value (n = 5). There was no close correlation between variations of depth of sleep and variations of sympathetic activity but during continuously deepening sleep MSA decreased progressively with time. In stage 2 sleep, high amplitude K complexes were accompanied by short-lasting increases of sympathetic activity. Since these increases of MSA were not preceded by decreases of diastolic blood pressure, which is known to evoke increased sympathetic nerve traffic in muscle nerves, we suggest that K complex related increases of MSA are signs of arousal which elicit both cortical EEG phenomena and activation of cerebral sympathetic centres. During desynchronized (REM) sleep, total MSA increased to 124 +/- 12% of the value in awake state (n = 5). The increases occurred mainly in short irregular periods, often related to rapid eye movements and there was an inverse relationship between the duration of the desynchronized sleep and the increase of total MSA. Our findings are similar to the data obtained in animal experiments and may partly explain changes of blood pressure during synchronized and desynchronized sleep reported previously in man.

Muscle nerve sympathetic activity (MSA), the interval between two R-waves in the ECG, or the interbeat interval (RR-interval), and blood pressure (BP) were recorded in 10 awake patients with obstructive sleep apnea (OSA) and in nine sex- and age-matched controls. Changes in RR-interval and MSA, evoked by sodium nitroprusside-induced reduction of BP, were used to quantitate baroreflex sensitivity. Both the cardiac (expressed as the RR-interval versus mean arterial BP slope) and the muscle sympathetic (mean MSA area versus diastolic BP slope) baroreflex sensitivity were depressed in patients as compared with controls. Cardiac baroreflex slope sensitivity (expressed as a regression coefficient) was 5.5 +/- 1.2 (mean +/- SEM) in patients and 9.6 +/- 0.96 in controls (p < 0.05). The corresponding figures for the sympathetic slope sensitivity were -4.9 +/- 0.9 and -13.1 +/- 2.3, respectively (p < 0.05). Differences remained after stepwise correction for age, body mass index (BMI), and to some extent BP. Resting MSA correlated with cardiac (r = 0.67, p < 0.003) and sympathetic (r = 0.56, p < 0.025) baroreflex sensitivity in the entire study group. We conclude that OSA patients exhibit an impaired baroreflex sensitivity to a hypotensive stimulus, which may represent an adaptive response to changes in BP or hypoxemia occurring in association with nocturnal apneas. Baroreflex adaptation may also contribute to the augmentation of resting MSA observed in OSA patients in this as well as in a previous study.