Changes in Muscle Sympathetic Nerve Activity, Venous Plasma Catecholamines, and Calf Vascular Resistance during Mechanical Ventilation with PEEP in Humans

1989 ◽  
Vol 70 (2) ◽  
pp. 243-250 ◽  
Author(s):  
Hans Selldén ◽  
Henrik Sjövall ◽  
B. Gunnar Wallin ◽  
Jan Häggendal ◽  
Sven-Erik Ricksten
Keyword(s):  
Mechanical Ventilation ◽  
Vascular Resistance ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Plasma Catecholamines ◽  
Nerve Activity ◽  
Venous Plasma

Abstract 019: Effect of CPAP on Blood Pressure and Central Sympathetic Outflow in Diabetic Patients with OSA, Resistant HTN, and CKD

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Marcel Ruzicka ◽  
Swapnil Hiremath ◽  
Frans H Leenens ◽  
Judith Leech ◽  
Shawn Aaron
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Plasma Catecholamines ◽  
Response To Treatment ◽  
Diabetic Patients ◽  
Nerve Activity ◽  
Sympathetic Hyperactivity ◽  
Obstructive Sleep

Introduction: Central sympathetic hyperactivity as assessed by muscle sympathetic nerve activity recordings is thought to play a crucial role in the development and maintenance of hypertension (HTN) in patients with obstructive sleep apnea (OSA). Decreases in daytime and nocturnal blood pressure (BP) in response to treatment with continuous positive airway pressure (CPAP) are paralleled by decreases in muscle sympathetic nerve activity (MSNA). Patients with chronic kidney disease (CKD) have high MSNA. Bilateral nephrectomy, but not renal transplantation normalizes MSNA indicating central sympathoexcitatory effects by renal afferents. The objective of this study was to assess to what extent is HTN driven by central sympathetic hyperactivity in patients with diabetic CKD, OSA, and resistant HTN. Thirteen patients (age 62.2±7.4 years) with diabetic CKD, resistant HTN defined as SBP on 24-hr ABPM above 135 mmHg while on 3 or more BP lowering drugs (including diuretic) with OSA, were randomized to therapeutic CPAP or non-therapeutic CPAP for one months. 24-hr ABPM, plasma catecholamines, aldosterone, and renin, and MSNA were assessed before and 1 months after randomization. Our results show (Table) that in contrast to sham CPAP, therapeutic CPAP decreased daytime and nighttime BP. In contrast, neither therapeutic nor sham CPAP caused any changes in MSNA and plasma catecholamines. In conclusion, decreases in BP in response to CPAP in patients with in diabetic CKD, despite maintained high MSNA, indicate other mechanism contributing to HTN in these patients as well as other central sympathoexcitatory pathways activated.

Contribution of perfusion pressure to vascular resistance response during head-up tilt

2001 ◽  
Vol 281 (1) ◽  
pp. H371-H375 ◽  
Author(s):  
Virginia A. Imadojemu ◽  
Mary E. J. Lott ◽  
Kevin Gleeson ◽  
Cynthia S. Hogeman ◽  
Chester A. Ray ◽  
...  
Keyword(s):  
Flow Velocity ◽  
Vascular Resistance ◽  
Femoral Artery ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Resistance Response ◽  
Head Up Tilt ◽  
Artery Flow

We measured brachial and femoral artery flow velocity in eight subjects and peroneal and median muscle sympathetic nerve activity (MSNA) in five subjects during tilt testing to 40°. Tilt caused similar increases in MSNA in the peroneal and median nerves. Tilt caused a fall in femoral artery flow velocity, whereas no changes in flow velocity were seen in the brachial artery. Moreover, with tilt, the increase in the vascular resistance employed (blood pressure/flow velocity) was greater and more sustained in the leg than in the arm. The ratio of the percent increase in vascular resistance in leg to arm was 2.5:1. We suggest that the greater vascular resistance effects in the leg were due to an interaction between sympathetic nerve activity and the myogenic response.

scholarly journals Regulation of muscle sympathetic nerve activity after bed rest deconditioning

2001 ◽  
Vol 280 (5) ◽  
pp. H2230-H2239 ◽  
Author(s):  
James A. Pawelczyk ◽  
Julie H. Zuckerman ◽  
C. Gunnar Blomqvist ◽  
Benjamin D. Levine
Keyword(s):  
Vascular Resistance ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Orthostatic Intolerance ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Bed Rest ◽  
Orthostatic Tolerance ◽  
Nerve Activity ◽  
Stimulus Response

Cardiovascular deconditioning reduces orthostatic tolerance. To determine whether changes in autonomic function might produce this effect, we developed stimulus-response curves relating limb vascular resistance, muscle sympathetic nerve activity (MSNA), and pulmonary capillary wedge pressure (PCWP) with seven subjects before and after 18 days of −6° head-down bed rest. Both lower body negative pressure (LBNP; −15 and −30 mmHg) and rapid saline infusion (15 and 30 ml/kg body wt) were used to produce a wide variation in PCWP. Orthostatic tolerance was assessed with graded LBNP to presyncope. Bed rest reduced LBNP tolerance from 23.9 ± 2.1 to 21.2 ± 1.5 min, respectively (means ± SE, P= 0.02). The MSNA-PCWP relationship was unchanged after bed rest, though at any stage of the LBNP protocol PCWP was lower, and MSNA was greater. Thus bed rest deconditioning produced hypovolemia, causing a shift in operating point on the stimulus-response curve. The relationship between limb vascular resistance and MSNA was not significantly altered after bed rest. We conclude that bed rest deconditioning does not alter reflex control of MSNA, but may produce orthostatic intolerance through a combination of hypovolemia and cardiac atrophy.

α-Adrenergic vascular responsiveness to sympathetic nerve activity is intact after head-down bed rest in humans

2004 ◽  
Vol 286 (1) ◽  
pp. R151-R157 ◽  
Author(s):  
Atsunori Kamiya ◽  
Daisaku Michikami ◽  
Satoshi Iwase ◽  
Junichiro Hayano ◽  
Toru Kawada ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Bed Rest ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Nerve Activity ◽  
Before And After ◽  
Vascular Responsiveness

Space-flight and its ground-based simulation model, 6° head-down bed rest (HDBR), cause cardiovascular deconditioning in humans. Because sympathetic vasoconstriction plays a very important role in circulation, we examined whether HDBR impairs α-adrenergic vascular responsiveness to sympathetic nerve activity. We subjected eight healthy volunteers to 14 days of HDBR and before and after HDBR measured calf muscle sympathetic nerve activity (MSNA; microneurography) and calf blood flow (venous occlusion plethysmography) during sympathoexcitatory stimulation (rhythmic handgrip exercise). HDBR did not change the increase in total MSNA ( P = 0.97) or the decrease in calf vascular conductance ( P = 0.32) during exercise, but it did augment the increase in calf vascular resistance ( P = 0.0011). HDBR augmented the transduction gain from total MSNA into calf vascular resistance, assessed as the least squares linear regression slope of vascular resistance on total MSNA (0.05 ± 0.02 before HDBR, 0.20 ± 0.06 U·min-1·burst-1after HDBR, P = 0.0075), but did not change the transduction gain into calf vascular conductance ( P = 0.41). Our data indicate that α-adrenergic vascular responsiveness to sympathetic nerve activity is preserved in the supine position after HDBR in humans.

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

2016 ◽  
Vol 43 (3) ◽  
pp. 206-212 ◽  
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.

Dissociation of muscle sympathetic nerve activity and leg vascular resistance in humans

2000 ◽  
Vol 279 (3) ◽  
pp. H1215-H1219 ◽  
Author(s):  
J. Kevin Shoemaker ◽  
Michael D. Herr ◽  
Lawrence I. Sinoway
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Femoral Artery ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Blood Velocity ◽  
Handgrip Exercise ◽  
Nerve Activity

We examined the hypothesis that the increase in inactive leg vascular resistance during forearm metaboreflex activation is dissociated from muscle sympathetic nerve activity (MSNA). MSNA (microneurography), femoral artery mean blood velocity (FAMBV, Doppler), mean arterial pressure (MAP), and heart rate (HR) were assessed during fatiguing static handgrip exercise (SHG, 2 min) followed by posthandgrip ischemia (PHI, 2 min). Whereas both MAP and MSNA increase during SHG, the transition from SHG to PHI is characterized by a transient reduction in MAP but sustained elevation in MSNA, facilitating separation of these factors in vivo. Femoral artery vascular resistance (FAVR) was calculated (MAP/MBV). MSNA increased by 59 ± 20% above baseline during SHG ( P < 0.05) and was 58 ± 18 and 78 ± 18% above baseline at 10 and 20 s of PHI, respectively ( P < 0.05 vs. baseline). Compared with baseline, FAVR increased 51 ± 22% during SHG ( P < 0.0001) but returned to baseline levels during the first 30 s of PHI, reflecting the changes in MAP ( P < 0.005) and not MSNA. It was concluded that control of leg muscle vascular resistance is sensitive to changes in arterial pressure and can be dissociated from sympathetic factors.

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