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.
Because of the clinical and experimental utility of continuous finger blood pressure measurements and the need for accuracy, we tested the performance of a new hydraulic device in 22 consecutive hypertensive subjects during physiological and pharmacological interventions. Ipsilateral brachial intra-arterial pressure was monitored during rest, Valsalva's maneuver, static handgrip, and mental arithmetic and after sublingual glyceryl trinitrate. In excess of 40,000 blood pressure values were analyzed. Average bias (intra-arterial minus finger blood pressure) was 8.2 +/- 17.0 mm Hg (mean +/- SD, P = NS) for systolic and 2.8 +/- 10.4 mm Hg (P = NS) for diastolic pressure. Two-way ANOVA of biases with subject and task factors showed a subject effect (P < .001). Intersubject and intrasubject standard deviations of bias were 13.8 and 9.8 mm Hg systolic and 8.7 and 5.7 diastolic, respectively. Linear drift (millimeters of mercury per minute) of finger pressure was greater (P < .001) for systolic than diastolic pressure during static exercise and math and after glyceryl trinitrate. Coefficients of determination for blood pressure ranged from 0.4 +/- 0.3 to 0.8 +/- 0.3 during the tasks. We conclude that (1) noninvasive finger blood pressure faithfully follows intra-arterial changes but with clinically relevant offsets, (2) this technique is best suited for assessing pressure changes, (3) physiological and pharmacological interventions do not consistently affect finger pressure accuracy, (4) many reports of finger blood pressure measuring devices are based on direct readings obtained with inadequate system response characteristics, and (5) the tested instrument falls short of the standard requirements (bias < or = 5 +/- 8 mm Hg) for devices that measure intermittently.
1. Psychological characteristics were studied in 25 hypertensives (mean and standard deviation of blood pressure 150/95 +/- 12/5 mmHg), who received blood pressure (BP) biofeedback (BFB). Personality factors and success in BFB-BP modifying ability were correlated and the predictive value of psychological factors was estimated. 2. Questionnaires consisted of a Locus of Control of Behaviour (LCB) scale, the Spielberger state trait anxiety inventory and the Framingham Type A personality inventory. 3. BP was monitored continuously from the finger by volume clamp plethysmography during eight BFB sessions, each with three trials of raising, ignoring and lowering systolic blood pressure (SP). 4. SP was raised/lowered by 12 +/- 11/6 +/- 9 mmHg and heart rate (HR) increased by 10 +/- 3.9/+ 1 +/- 6.1. Ten subjects were able to lower SP by greater than or equal to 5 mmHg (15 +/- 7.5) and raise it by 17 +/- 11. The others achieved no decrease in SP and were also less successful at raising (8 mmHg, P = 0.04). 5. Changes in LCB and trait anxiety correlated with DP rise, whereas type A and pre-study state anxiety correlated with rising HR. Lowering of SP correlated weakly with change in LCB (r = 0.47, P = 0.06). 6. Combinations of psychological factors had independent predictive value for BP and HR change: trait anxiety (P = 0.03) and change in LCB (P = 0.009) with rise in diastolic blood pressure (DP); type A (P = 0.009), pre-study LCB (P = 0.02) and pre-study state anxiety (P = 0.01) with HR rise.(ABSTRACT TRUNCATED AT 250 WORDS)
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