Sympathetic and Hemodynamic Effects of Moderate and Deep Sedation with Propofol in Humans

Background The objective of this study was to determine the mechanisms involved in the hypotension associated with sedative doses of propofol in humans. Methods Ten healthy volunteers (aged 21-37 yr) participated on two occasions and in random order received placebo or propofol infusions. Standard monitoring and radial artery blood pressure were combined with measurement of forearm blood flow (plethysmography) and derivation of forearm vascular resistance, recording of peroneal nerve sympathetic activity, and blood sampling for norepinephrine concentrations. A computer-controlled infusion pump delivered placebo or two concentrations of propofol, adjusted to achieve moderate and deep sedation based on the Observer Assessment of Alertness/Sedation score (responsiveness component) of 4 and 3. Level of sedation was quantitated using bispectral analysis of the electroencephalogram. Baroreflexes were assessed with a hypotensive challenge via administration of sodium nitroprusside. Results Baseline neurocirculatory and respiratory parameters did not differ between sessions. Progressive infusions to achieve moderate and deep sedation resulted in average Bispectral Index values of 70 and 54, respectively. Propofol significantly reduced sympathetic nerve activity at both levels of sedation and decreased norepinephrine and forearm vascular resistance at deep sedation. These effects resulted in significant decreases in mean blood pressure of 9% and 18% at moderate and deep sedation, respectively. Propofol also reduced reflex increases in sympathetic nerve activity. Conclusions These data from healthy subjects indicate that sedation doses of propofol, which did not compromise respiratory function, had substantial inhibitory effects on sympathetic nerve activity and reflex responses to hypotension resulting in vasodilation and significant decreases in mean blood pressure.

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Effect of dietary potassium on blood pressure, renal function, muscle sympathetic nerve activity, and forearm vascular resistance and flow in normotensive and borderline hypertensive humans.

Circulation ◽

10.1161/01.cir.81.1.173 ◽

1990 ◽

Vol 81 (1) ◽

pp. 173-184 ◽

Cited By ~ 22

Author(s):

W J Lawton ◽

A E Fitz ◽

E A Anderson ◽

C A Sinkey ◽

R A Coleman

Keyword(s):

Blood Pressure ◽

Renal Function ◽

Vascular Resistance ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Muscle Sympathetic Nerve Activity ◽

Nerve Activity ◽

Dietary Potassium ◽

Forearm Vascular Resistance

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Closed loop heart beat interval modelization in humans using mean blood pressure, instantaneous lung volume and muscle sympathetic nerve activity

Proceedings of 18th Annual International Conference of the IEEE Engineering in Medicine and Biology Society ◽

10.1109/iembs.1996.647559 ◽

2002 ◽

Cited By ~ 1

Author(s):

P. Celka ◽

R. Vetter ◽

U. Scherrer ◽

E. Pruvot

Keyword(s):

Blood Pressure ◽

Lung Volume ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Closed Loop ◽

Muscle Sympathetic Nerve Activity ◽

Heart Beat ◽

Mean Blood Pressure ◽

Nerve Activity

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Importance of left atrial baroreceptors in the cardiopulmonary baroreflex of normal humans

Journal of Applied Physiology ◽

10.1152/jappl.1993.74.6.2672 ◽

1993 ◽

Vol 74 (6) ◽

pp. 2672-2680 ◽

Cited By ~ 26

Author(s):

R. M. Oren ◽

H. P. Schobel ◽

R. M. Weiss ◽

W. Stanford ◽

D. W. Ferguson

Keyword(s):

Computed Tomography ◽

Vascular Resistance ◽

Sympathetic Nerve ◽

Left Atrial ◽

Sympathetic Nerve Activity ◽

Nerve Activity ◽

Cardiopulmonary Baroreflex ◽

Normal Humans ◽

Cardiac Filling ◽

Forearm Vascular Resistance

In animals, sympathetic responses to orthostasis are regulated in part by cardiopulmonary afferents arising from atrial and ventricular baroreceptors. To determine the relative importance of these baroreceptor regions in the cardiopulmonary baroreflex of normal humans, simultaneous measurements of left atrial and right and left ventricular volumes (cine computed tomography), invasive hemodynamics, forearm vascular resistance (plethysmography), and efferent sympathetic nerve activity to muscle (microneurography) were obtained under control conditions and with nonhypotensive lower body negative pressure (-10 mmHg, LBNP-10) in nine normal human subjects. LBNP-10 did not alter heart rate or mean systemic arterial pressure, but it did produce significant decreases in pulmonary artery diastolic and right atrial pressures. This reduction in cardiac filling pressures resulted in efferent sympathoexcitation evidenced by increases in forearm vascular resistance and efferent sympathetic nerve activity to the muscle. LBNP-10 did not alter end-diastolic volume of the left or the right ventricle. Similarly, ventricular stroke volume was unchanged during LBNP-10, as assessed by cine computed tomography or thermodilution techniques. In contrast, LBNP-10 resulted in a significant decrease in left atrial volume. Thus, LBNP produced a significant decrease in cardiac filling pressures and left atrial volumes with resultant reflex sympathoexcitation, whereas ventricular volumes were unchanged. These observations suggest an important role for left atrial (nonventricular) baroreceptor afferents in the cardiopulmonary baroreflex of normal humans.

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Post-Exercise Hypotension Is Mediated by a Decrease in Sympathetic Nerve Activity in Stages 2-3 CKD

American Journal of Nephrology ◽

10.1159/000445443 ◽

2016 ◽

Vol 43 (3) ◽

pp. 206-212 ◽

Cited By ~ 5

Author(s):

Daniele C.B. Aprile ◽

Bruna Oneda ◽

Josiane L. Gusmão ◽

Luiz A.R. Costa ◽

Claudia L.M. Forjaz ◽

...

Keyword(s):

Aerobic Exercise ◽

Vascular Resistance ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Muscle Sympathetic Nerve Activity ◽

Random Order ◽

Peak Oxygen Uptake ◽

Cycle Ergometer ◽

Control Group ◽

Nerve Activity

Background: This study aimed at evaluating the after effects of a single bout of aerobic exercise on muscle sympathetic nerve activity (MSNA), peripheral vascular resistance and blood pressure (BP) in stages 2-3 chronic kidney disease (CKD) patients. We hypothesized that CKD patients present a greater decline in these variables after the exercise than healthy individuals. Methods: Nine patients with stages 2-3 CKD (50 ± 8 years) and 12 healthy volunteers (50 ± 5 years) underwent 2 sessions, conducted in a random order: exercise (45 min, cycle ergometer, 50% of peak oxygen uptake) and rest (seated, 45 min). Sixty minutes after either intervention, MSNA (by microneurography), BP (by oscillometry), and forearm vascular resistance (FVR) were measured. A 2-way analysis of variance with group (between) and session (within) as main factors was employed, accepting p < 0.05 as significant. Results: Diastolic BP and MSNA were higher in the CKD than the control group in both sessions. Responses after exercise were similar in both groups. Systolic BP, diastolic BP, MSNA and FVR were significantly lower after the exercise than after the rest session in both the CKD and the control groups (162 ± 15 vs. 152 ± 23 and 155 ± 11 vs. 145 ± 16 mm Hg, 91 ± 11 vs. 85 ± 14 and 77 ± 5 vs. 71 ± 10 mm Hg, 38 ± 4 vs. 31 ± 4 and 34 ± 2 vs. 27 ± 4 burst/min, 59 ± 29 vs. 41 ± 29 and 45 ± 20 vs. 31 ± 8 U, respectively, all p < 0.05). Conclusion: These results showed that aerobic exercise may produce hemodynamic and neural responses that can be beneficial to these patients in spite of CKD.

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Modulation of cardiovascular reflexes by arginine vasopressin

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y87-270 ◽

1987 ◽

Vol 65 (8) ◽

pp. 1717-1723 ◽

Cited By ~ 5

Author(s):

John S. Floras ◽

Philip E. Aylward ◽

Badri N. Gupta ◽

Allyn L. Mark ◽

Francois M. Abboud

Keyword(s):

Arterial Pressure ◽

Vascular Resistance ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Venous Pressure ◽

Left Ventricular ◽

Nerve Activity ◽

Baroreflex Control ◽

Normal Humans ◽

Forearm Vascular Resistance

Arginine vasopressin (AVP), a potent vasoconstrictor, does not raise arterial pressure in normal humans or neurally intact animals, even during infusions that achieve pathophysiological plasma concentrations. It has been proposed that this is because AVP facilitates the baroreflex control of the circulation. We performed a series of investigations to test this hypothesis, and to determine sites at which AVP might act to augment the baroreflex. In anesthetized rabbits, vasopressin (36 pmol∙kg−1∙min−1) increased discharge from both medullated and nonmedullated single fibres from aortic baroreceptor nerves during elevations in aortic arch pressure. Similarly, vasopressin (36 pmol∙kg−1∙min−1) increased the response of left ventricular mechanoreceptor single fibre discharge to elevations of left ventricular end-diastolic pressure. These observations suggest that sensitization of high and low pressure baroreceptors is one mechanism by which vasopressin may facilitate baroreflexes. In a further series of experiments in sinoaortic denervated anesthetized rabbits, vasopressin (18 pmol∙kg−1∙min−1) facilitated vagally mediated reflex inhibition of renal sympathetic nerve activity during volume expansion. In humans, AVP (0.37 pmol∙kg−1∙min−1) raised plasma AVP to an antidiuretic level (22 ± 4 fmol/mL), but did not change blood pressure or the baroreflex control of heart rate or forearm vascular resistance. A higher dose (3.7 pmol∙kg−1∙min−1) raised plasma levels to 268 ± 38 fmol/mL, decreased pulse pressure, increased central venous pressure (from 2.6 ± 0.5 to 4.1 ± 0.4 mmHg) (1 mmHg = 133.3 Pa) and suprisingly, in view of its direct vasoconstrictor effect, increased forearm blood flow by 30% and decreased forearm vascular resistance from 24 ± 4 to 18 ± 3 units (p < 0.05); mean arterial pressure was unchanged. The reflex vasodilator response to the sudden release of lower body negative pressure was augmented by AVP, whereas reflex changes in heart rate were unaltered. To test the hypothesis that vasopressin caused this resting vasodilation through inhibition of sympathetic nerve activity, we recorded postganglionic efferent muscle sympathetic nerve activity directly from the peroneal nerve before, during, and after intravenous infusion of AVP, 3.7 pmol∙kg−1∙min−1. Forearm vascular resistance again fell; sympathetic nerve activity decreased abruptly on starting AVP, from 254 ± 40 to 163 ± 34 units (p < 0.05), and remained below control throughout the infusion. This decrease did not appear to be due to a ganglionic action of AVP. The inhibition of sympathetic nerve activity probably resulted principally from mechanical stimulation of cardiac and arterial baroreceptors. However, since the marked reduction of nerve activity was not consistently associated with increases in arterial pressure or central venous pressure, we cannot exclude the possibility that vasopressin decreased sympathetic nerve activity in part by sensitizing baroreceptor afferents or by a central neural action. Sympathoinhibition would appear to be an important mechanism by which the potent pressor effects of AVP are countered in normal humans.

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