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Plasma Noradrenaline (plasma + noradrenaline)
Selected AbstractsForearm vascular and neuroendocrine responses to graded water immersion in humansACTA PHYSIOLOGICA, Issue 2 2000Gabrielsen The hypothesis that graded expansion of central blood volume by water immersion to the xiphoid process and neck would elicit a graded decrease in forearm vascular resistance was tested. Central venous pressure increased (P < 0.05) by 4.2 ± 0.4 mmHg (mean ± SEM) during xiphoid immersion and by 10.4 ± 0.5 mmHg during neck immersion. Plasma noradrenaline was gradually suppressed (P < 0.05) by 62 ± 8 and 104 ± 11 pg mL,1 during xiphoid and neck immersion, respectively, indicating a graded suppression of sympathetic nervous activity. Plasma concentrations of arginine vasopressin were suppressed by 1.5 ± 0.5 pg mL,1 (P < 0.05) during xiphoid immersion and by 2.0 ± 0.5 pg mL,1 during neck immersion (P < 0.05 vs. xiphoid immersion). Forearm subcutaneous vascular resistance decreased to the same extent by 26 ± 9 and 28 ± 4% (P < 0.05), respectively, during both immersion procedures, whereas forearm skeletal muscle vascular resistance declined only during neck immersion by 27 ± 6% (P < 0.05). In conclusion, graded central blood volume expansion initiated a graded decrease in sympathetic nervous activity and AVP-release. Changes in forearm subcutaneous vascular resistance, however, were not related to the gradual withdrawal of the sympathetic and neuroendocrine vasoconstrictor activity. Forearm skeletal muscle vasodilatation exhibited a more graded response with a detectable decrease only during immersion to the neck. Therefore, the forearm subcutaneous vasodilator response reaches saturation at a lower degree of central volume expansion than that of forearm skeletal muscle. [source] Systemic nitric oxide clamping in normal humans guided by total peripheral resistanceACTA PHYSIOLOGICA, Issue 2 2010J. A. Simonsen Abstract Aim:, We wanted to stabilize the availability of nitric oxide (NO) at levels compatible with normal systemic haemodynamics to provide a model for studies of complex regulations in the absence of changes in NO levels. Methods:, Normal volunteers (23,28 years) were infused i.v. with the nitric oxide synthase (NOS) inhibitor NG -nitro- l -arginine methyl ester (l -NAME) at 0.5 mg kg,1 h,1. One hour later, the NO donor sodium nitroprusside (SNP) was co-infused in doses eliminating the haemodynamic effects of l -NAME. Haemodynamic measurements included blood pressure (MABP) and cardiac output (CO) by impedance cardiography. Results:,l -NAME increased MABP and total peripheral resistance (TPR, 1.02 ± 0.05 to 1.36 ± 0.07 mmHg s mL,1, mean ± SEM, P < 0.001). With SNP, TPR fell to a stable value slightly below control (0.92 ± 0.05 mmHg s mL,1, P < 0.05). CO decreased with l -NAME (5.8 ± 0.3 to 4.7 ± 0.3 L min,1, P < 0.01) and returned to control when SNP was added (6.0 ± 0.3 L min,1). A decrease in plasma noradrenaline (42%, P < 0.01) during l -NAME administration was completely reversed by SNP. Plasma renin activity decreased during l -NAME administration and returned towards normal after addition of SNP. In contrast, plasma aldosterone was increased by l -NAME and remained elevated. Conclusions:, Concomitant NOS inhibition and NO donor administration can be adjusted to maintain TPR at control level for hours. This approach may be useful in protocols in which stabilization of the peripheral supply of NO is required. However, the dissociation between renin and aldosterone secretion needs further investigation. [source] No effect of venoconstrictive thigh cuffs on orthostatic hypotension induced by head-down bed restACTA PHYSIOLOGICA, Issue 2 2000M.-A. Custaud Orthostatic intolerance (OI) is the most serious symptom of cardiovascular deconditioning induced by head-down bed rest or weightlessness. Wearing venoconstrictive thigh cuffs is an empirical countermeasure used by Russian cosmonauts to limit the shift of fluid from the lower part of the body to the cardio-cephalic region. Our aim was to determine whether or not thigh cuffs help to prevent orthostatic hypotension induced by head-down bed rest. We studied the effect of thigh cuffs on eight healthy men. The cuffs were worn during the day for 7 days of head-down bed rest. We measured: orthostatic tolerance (stand tests and lower body negative pressure tests), plasma volume (Evans blue dilution), autonomic influences (plasma noradrenaline) and baroreflex sensitivity (spontaneous baroreflex slope). Thigh cuffs limited the loss of plasma volume (thigh cuffs: ,201 ± 37 mL vs. control: ,345 ± 42 mL, P < 0.05), the degree of tachycardia and reduction in the spontaneous baroreflex sensitivity induced by head-down bed rest. However, the impact of thigh cuffs was not sufficient to prevent OI (thigh cuffs: 7.0 min of standing time vs. control: 7.1 min). Decrease in absolute plasma volume and in baroreflex sensitivity are known to be important factors in the aetiology of OI induced by head-down bed rest. However, dealing with these factors, using thigh cuffs for example, is not sufficient to prevent OI. Other factors such as venous compliance, microcirculatory changes, peripheral arterial vasoconstriction and vestibular afferents must also be considered. [source] Forearm vasoconstrictor response in uncomplicated type 1 diabetes mellitusEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 10 2006P. J. Van Gurp Abstract Background, According to the ,haemodynamic hypothesis', increased tissue perfusion predisposes to microangiopathy in diabetic patients. We hypothesized that the typical haemodynamic changes underlying the increased tissue perfusion can be explained by a decreased sympathetic nerve activity caused by chronic hyperglycaemia. In this study we investigated sympathetic activity in patients with uncomplicated type 1 diabetes mellitus (DM). Materials and methods, In 15 DM patients (DM duration 6·3 ± 3·8 year; HbA1c 7·9 ± 1·3%) and 16 age- and sex-matched healthy volunteers (Control), sympathetic nervous system activity was measured at rest (baseline) and during sympathoneural stimulation (lower body negative pressure (LBNP)) by means of interstitial and plasma noradrenaline (NA) sampling and power spectral analysis. Muscle sympathetic nerve activity (MSNA) was measured before (baseline) and during a cold pressure test. Forearm blood flow was measured during forearm vascular ,- and ,-adrenergic receptor blockade. Results, At baseline, forearm vascular resistance (FVR), plasma NA concentrations, MSNA and heart rate variability were similar in both groups. LBNP-induced vasoconstriction was significantly attenuated in the DM group compared with the Control group (,FVR: 12 ± 4 vs. 19 ± 3 arbitrary units, P < 0·05). The responses of plasma NA and heart rate variability did not differ. Conclusions,, Baseline FVR and sympathetic nerve activity are normal in patients with uncomplicated type 1 diabetes. However, the forearm vasoconstrictor response to sympathetic stimulation is attenuated, which cannot be attributed to an impaired sympathetic responsiveness. [source] Daytime sympathetic hyperactivity in OSAS is related to excessive daytime sleepinessJOURNAL OF SLEEP RESEARCH, Issue 3 2007VINCENZO DONADIO Summary The aim of this study was to investigate the relationships among sympathetic hyperactivity, excessive daytime sleepiness (EDS) and hypertension in obstructive sleep apnoea syndrome (OSAS). Ten newly diagnosed OSAS patients with untreated EDS and daytime hypertension underwent polysomnography (PSG) and daytime measurements of plasma noradrenaline (NA), ambulatory blood pressure (BP), muscle sympathetic nerve activity (MSNA) by microneurography and objective assessment of EDS before and during 6 months of compliance-monitored continuous positive airway pressure (CPAP) treatment. One month after the start of CPAP, BP, MSNA and NA were significantly lowered, remaining lower than baseline also after 3 and 6 months of treatment. CPAP use caused a significant improvement of sleep structures, and reduced EDS. A statistical correlation analysis demonstrated that EDS was not correlated with sleep measures obtained from baseline PSG (% sleep stages, apnoea and arousal index, mean oxygen saturation value), whereas daytime sleepiness was significantly correlated with MSNA. Furthermore, MSNA and BP showed no correlation. Our data obtained from selected patients suggest that the mechanisms inducing EDS in OSAS are related to the degree of daytime sympathetic hyperactivity. Additionally, resting MSNA was unrelated to BP suggesting that factors other than adrenergic neural tone make a major contribution to OSAS-related hypertension. The results obtained in this pilot study need, however, to be confirmed in a larger study involving more patients. [source] Abnormality of the Left Ventricular Sympathetic Nervous Function Assessed by I-123 Metaiodobenzylguanidine Imaging in Pediatric Patients with Neurocardiogenic SyncopePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 10 2003RANA OLGUNTÜRK The purpose of this study was to assess the left ventricular sympathetic nervous system function in the patients with neurocardiogenic syncope (NCS) using I-123 metaiodobenzylguanidine (MIBG) imaging of the heart, and to compare the plasma noradrenaline (NA) and MIBG results of tilt positive and tilt negative patients following a head-up tilt test (HUT). The study included 30 patients. Their physical and laboratory examinations did not show a pathology that may be the cause of their syncope. HUT test was positive in 13 patients and negative in 17 patients. Plasma NA concentrations were higher in the HUT positive than the HUT negative group at the beginning and at the 10th minute of the test. Specific I-123 MIBG uptake assessed as the cardiac to mediastinal activity ratio in the delayed image was significantly higher in HUT positive group. The higher levels of MIBG uptake and plasma NA observed in HUT positive patients may reflect the greater capacity of NA storage in cardiac adrenergic neuronal tissue in patients with NCS. The results of this study support the critical role of autonomic nervous system in the pathophysiology of NCS and the excessive sympathetic nervous stimulation as the trigger of paradox reflex. (PACE 2003; 26:1926,1930) [source] Mathematical modeling of the circadian rhythm of key neuroendocrine,immune system players in rheumatoid arthritis: A systems biology approachARTHRITIS & RHEUMATISM, Issue 9 2009Michael Meyer-Hermann Objective Healthy subjects and patients with rheumatoid arthritis (RA) exhibit circadian rhythms of the neuroendocrine,immune system. Understanding circadian dynamics is complex due to the nonlinear behavior of the neuroendocrine,immune network. This study was undertaken to seek and test a mathematical model for studying this network. Methods We established a quantitative computational model to simulate nonlinear interactions between key factors in the neuroendocrine,immune system, such as plasma tumor necrosis factor (TNF), plasma cortisol (and adrenal cholesterol store), and plasma noradrenaline (NA) (and presynaptic NA store). Results The model was nicely fitted with measured reference data on healthy subjects and RA patients. Although the individual circadian pacemakers of cortisol, NA, and TNF were installed without a phase shift, the relative phase shift between these factors evolved as a consequence of the modeled network interactions. Combined long-term and short-term TNF increase (the "RA model") increased cortisol plasma levels for only a few days, and cholesterol stores started to become markedly depleted. This nicely demonstrated the phenomenon of inadequate cortisol secretion relative to plasma TNF levels, as a consequence of adrenal deficiency. Using the RA model, treatment with glucocorticoids between midnight and 2:00 AM was found to have the strongest inhibitory effect on TNF secretion, which supports recent studies on RA therapy. Long-term reduction of TNF levels by simulation of anti-TNF therapy normalized cholesterol stores under "RA" conditions. Conclusion These first in silico studies of the neuroendocrine,immune system in rheumatology demonstrate that computational biology in medicine, making use of large collections of experimental data, supports understanding of the pathophysiology of complex nonlinear systems. [source] Human in vivo study of the renin,angiotensin,aldosterone system and the sympathetic activity after 8 weeks daily intake of fermented milkCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 2 2010Lotte Usinger Summary Objective:, Milk fermented by lactic acid bacteria is suggested to have antihypertensive effect in humans. In vitro and animal studies have established an angiotensin-converting enzyme (ACE) inhibitor effect of peptides in fermented milk. However, other modes of action must be considered, because until today no human studies have confirmed an ACE inhibition in relation to the intake of fermented milk. Materials and methods:, We undertook a double-blinded randomized placebo-controlled study including 94 borderline-hypertensive persons to study the effect on human physiology of Lactobacillus helveticus fermented milk. The subjects were randomized into three groups: Cardi04-300 ml, Cardi04-150 ml or placebo. All components of the renin,angiotensin,aldosterone system were measured several times. Sympathetic activity was estimated by plasma noradrenaline and cardiovascular response to head-up tilt at baseline and after 8 weeks of intervention. Results:, No ACE inhibition of the fermented milk was demonstrated, as none of the components of the renin,angiotensin,aldosteron system changed. Plasma noradrenaline response to tilt test after intervention stayed unchanged between groups (P = 0·38), but declined in the group Cardi04-300 from 2·01 ± 0·93 nmol l,1 at baseline to 1·49 ± 0·74 nmol l,1 after 8 weeks (P = 0·002). There was no change in 24-h ambulatory blood pressure or heart rate between groups. Conclusions:, Despite a known ACE inhibitory effect in vitro and in animals, milk fermented with Lb. helveticus did not inhibit ACE in humans. Our results suggest that the intake of fermented milk decreases sympathetic activity, although not to an extent mediating reductions of blood pressure and heart rate in borderline-hypertensive subjects. [source] | ||||||||||