scholarly journals COULD PLASMA ADRENALINE DURING COLD PRESSOR TEST BE USED TO IDENTIFY PATIENTS WHO RESPOND TO RENAL DENERVATION?

2019 ◽  
Vol 37 ◽  
pp. e220
Author(s):  
O. Undrum Bergland ◽  
C. Søraas ◽  
A. Larstorp ◽  
A. Høieggen ◽  
M. Rostrup ◽  
...  
1981 ◽  
Vol 61 (s7) ◽  
pp. 161s-164s ◽  
Author(s):  
P. Bolli ◽  
F. W. Amann ◽  
L. Hulthén ◽  
W. Kiowski ◽  
F. R. Bühler

1. Stressful sympathetic stimulation (cold pressor test) was applied to 18 patients with essential hypertension and 15 normotensive subjects. Intra-arterial blood pressure, heart rate, plasma adrenaline and noradrenaline concentrations as well as forearm blood flow were measured before and during the cold pressor test; tests were repeated after regional postsynaptic α1-adrenoceptor blockade with prazosin. 2. Under basal conditions mean blood pressure (P < 0.001), heart rate (P < 0.01), forearm blood flow (P < 0.001) as well as adrenaline concentration (P < 0.01), but not noradrenaline, was higher in patients with essential hypertension. 3. During the cold pressor test, mean blood pressure, heart rate, plasma adrenaline and noradrenaline concentrations increased and forearm flow decreased (all P < 0.001). 4. Stress-stimulated plasma adrenaline was higher in essential hypertensive patients than in normotensive subjects (P < 0.01). In the former the stress-induced increase in plasma adrenaline correlated with the increase in mean blood pressure (r = 0.514; P < 0.05). 5. Prazosin increased forearm blood flow more in essential hypertension (P < 0.001). This increase correlated with the resting plasma adrenaline in the hypertensive (r = 0.710; P < 0.001), but not in normotensive, subjects. 6. When the cold pressor test was repeated during postsynaptic α1-adrenoceptor blockade forearm blood flow did not decrease; instead it increased further in both groups (P < 0.05). 7. Thus in essential hypertension elevated plasma adrenaline concentration reflects sympathetic overactivity as also expressed by enhanced α-adrenoceptor-mediated vasoconstriction.


1989 ◽  
Vol 76 (6) ◽  
pp. 625-630 ◽  
Author(s):  
P. M. G. Bouloux ◽  
E. Newbould ◽  
R. Causon ◽  
L. Perry ◽  
L. H. Rees ◽  
...  

1. Although the opiate antagonist naloxone has been shown to affect sympathoadrenomedullary function in some studies, this has not been a uniform finding in all investigations, using different doses of naloxone. We have therefore investigated the actions of saline placebo and increasing bolus doses of intravenous naloxone (25, 100 and 250 μg/kg) on the plasma noradrenaline, adrenaline, adrenocorticotrophin (ACTH) and cortisol responses to a cold-pressor test in six males and two females in a double-blind randomized study. 2. Basal levels of adrenaline did not differ on any of the study occasions: the cold-pressor stimulus produced a significant rise in mean plasma adrenaline to a peak of 0.16 nmol/l, with a peak incremental rise of 0.08 nmol/l. In the presence of the two higher doses of naloxone, the incremental rise in the mean adrenaline level was significantly enhanced, reaching 0.30 nmol/l at 100 μg of naloxone/kg and 0.29 nmol/l at 250 μg of naloxone/kg, with no significant enhancement observed at the lowest dose of naloxone. The rise in plasma noradrenaline, systolic and diastolic blood pressure and pulse rate during the cold-pressor test was not consistently altered by any dose of naloxone, but there was a significant trend for the degree of discomfort to increase with the dose of naloxone. 3. Neither plasma ACTH nor serum cortisol rose in response to the cold-pressor stimulus. Analysis of variance demonstrated a significant naloxone-treatment effect for both ACTH and cortisol, with the 100 μg/kg and 250 μg/kg doses of naloxone leading to a significant rise in mean plasma ACTH not seen at the lowest dose of 25 μg/kg. 4. In a separate study of the effect of naloxone on the clearance of plasma adrenaline, adrenaline was infused on two occasions into eight normal male subjects to a maximum dose of 5 μg/min for 15 min, and blood was sampled at regular intervals during and after termination of the infusion, preceded by 8 mg of naloxone or placebo. After termination of the adrenaline infusion, there was a rapid fall in plasma adrenaline (Λ = −1.9 ± 0.3 min), which was not altered by naloxone (Λ = −1.8 ± 0.3 min). 5. We conclude that the potentiation of the adrenaline response to a cold-pressor test by naloxone is mediated by increased secretion of adrenaline and not by a reduction in its clearance rate, and that this response is of low naloxone sensitivity.


1985 ◽  
Vol 69 (3) ◽  
pp. 365-368 ◽  
Author(s):  
Pierre-Marc Bouloux ◽  
Ashley Grossman ◽  
Saad Al-Damluji ◽  
Timothy Bailey ◽  
Michael Besser

1. The effects of naloxone (8 mg) on the pressor and plasma catecholamine response to a standard cold-pressor test have been evaluated in six normal male subjects. Plasma catecholamines were estimated by high performance liquid chromatography coupled to electrochemical detection. 2. Cold stimulation induced significant elevations in plasma noradrenaline and adrenaline to reach mean peak levels 61% and 108% above their respective basal levels (P < 0.05). Systolic blood pressure increased by 23 ± 6.5 mmHg (P < 0.001), and heart rate increased by 7.5 ± 2.5 beats/min (P < 0.001). 3. Naloxone pretreatment significantly enhanced the plasma adrenaline response to the cold stimulus by 98% (P < 0.01) with concomitant changes in peak systolic blood pressure (peak increment 31 ± 6 mmHg) and pulse rate (12.5 ± 3.5 beats/min) responses (both P < 0.05). The mean plasma noradrenaline response to cold also increased after naloxone, but this failed to achieve significance. 4. Endogenous opioids are likely to be involved in the sympathoadrenal response to a mild acute stress in man.


2016 ◽  
Vol 14 (4) ◽  
Author(s):  
Marcelo Coertjens

Introdução: A crioterapia é um recurso que diminui a temperatura corporal local com finalidades terapêuticas. Uma importante repercussão é a vasoconstrição local, que seria o desencadeador de um possível aumento na pressão arterial (PA). Entretanto, não existem trabalhos que comprovem essa suposição. Nossa hipótese é que os resultados das pesquisas de Cold Pressor Test (CPT) avaliando PA acabaram historicamente fundamentando as precauções da crioterapia em relação a pacientes hipertensos. Objetivo: Realizar uma revisão de literatura a respeito das pesquisas que sustentam a precaução da crioterapia em indivíduos hipertensos e verificar sua relação com estudos que utilizaram o CPT. Material e métodos: Trata-se de uma revisão de literatura que utilizou as bases de dados online Medline, Scielo, Lilacs e Google Acadêmico para a realização da pesquisa. Resultado: Apesar de não serem unânimes, diversas pesquisas que utilizaram o CPT encontraram significativos aumentos da atividade nervosa simpática muscular e da PA em normotensos e hipertensos, entretanto não encontramos estudos que tenham comprovado respostas significativas de PA com o uso da crioterapia, principalmente, em hipertensos. Conclusão: Não existem evidências científicas que comprovem a precaução da crioterapia em indivíduos hipertensos. Além disso, os estudos com CPT não são unânimes em relação aos aumentos pressóricos em indivíduos normotensos e hipertensos.Palavras-chave: crioterapia, hemodinâmica, hipertensão, pressão arterial. 


Author(s):  
Guillaume Lamotte ◽  
Christopher J. Boes ◽  
Phillip A. Low ◽  
Elizabeth A. Coon

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Morten Pallisgaard Støve ◽  
Rogerio Pessoto Hirata ◽  
Thorvaldur Skuli Palsson

Abstract Objectives The effect of stretching on joint range of motion is well documented, and although sensory perception has significance for changes in the tolerance to stretch following stretching the underlining mechanisms responsible for these changes is insufficiently understood. The aim of this study was to examine the influence of endogenous pain inhibitory mechanisms on stretch tolerance and to investigate the relationship between range of motion and changes in pain sensitivity. Methods Nineteen healthy males participated in this randomized, repeated-measures crossover study, conducted on 2 separate days. Knee extension range of motion, passive resistive torque, and pressure pain thresholds were recorded before, after, and 10 min after each of four experimental conditions; (i) Exercise-induced hypoalgesia, (ii) two bouts of static stretching, (iii) resting, and (iv) a remote, painful stimulus induced by the cold pressor test. Results Exercise-induced hypoalgesia and cold pressor test caused an increase in range of motion (p<0.034) and pressure pain thresholds (p<0.027). Moderate correlations in pressure pain thresholds were found between exercise-induced hypoalgesia and static stretch (Rho>0.507, p=0.01) and exercise-induced hypoalgesia and the cold pressor test (Rho=0.562, p=0.01). A weak correlation in pressure pain thresholds and changes in range of motion were found following the cold pressor test (Rho=0.460, p=0.047). However, a potential carryover hypoalgesic effect may have affected the results of the static stretch. Conclusions These results suggest that stretch tolerance may be linked with endogenous modulation of pain. Present results suggest, that stretch tolerance may merely be a marker for pain sensitivity which may have clinical significance given that stretching is often prescribed in the rehabilitation of different musculoskeletal pain conditions where reduced endogenous pain inhibition is frequently seen.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kilin Shi ◽  
Tobias Steigleder ◽  
Sven Schellenberger ◽  
Fabian Michler ◽  
Anke Malessa ◽  
...  

AbstractContactless measurement of heart rate variability (HRV), which reflects changes of the autonomic nervous system (ANS) and provides crucial information on the health status of a person, would provide great benefits for both patients and doctors during prevention and aftercare. However, gold standard devices to record the HRV, such as the electrocardiograph, have the common disadvantage that they need permanent skin contact with the patient. Being connected to a monitoring device by cable reduces the mobility, comfort, and compliance by patients. Here, we present a contactless approach using a 24 GHz Six-Port-based radar system and an LSTM network for radar heart sound segmentation. The best scores are obtained using a two-layer bidirectional LSTM architecture. To verify the performance of the proposed system not only in a static measurement scenario but also during a dynamic change of HRV parameters, a stimulation of the ANS through a cold pressor test is integrated in the study design. A total of 638 minutes of data is gathered from 25 test subjects and is analysed extensively. High F-scores of over 95% are achieved for heartbeat detection. HRV indices such as HF norm are extracted with relative errors around 5%. Our proposed approach is capable to perform contactless and convenient HRV monitoring and is therefore suitable for long-term recordings in clinical environments and home-care scenarios.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Andreas M. Weng ◽  
Herbert Köstler ◽  
Thorsten A. Bley ◽  
Christian O. Ritter

Abstract Background The effect of smoking on coronary vasomotion has been investigated in the past with various imaging techniques in both short- and long-term smokers. Additionally, coronary vasomotion has been shown to be normalized in long-term smokers by L-Arginine acting as a substrate for NO synthase, revealing the coronary endothelium as the major site of abnormal vasomotor response. Aim of the prospective cohort study was to investigate coronary vasomotion of young healthy short-term smokers via magnetic resonance cold pressor test with and without the administration of L-Arginine and compare obtained results with the ones from nonsmokers. Methods Myocardial blood flow (MBF) was quantified with first-pass perfusion MRI on a 1.5 T scanner in healthy short-term smokers (N = 10, age: 25.0 ± 2.8 years, 5.0 ± 2.9 pack years) and nonsmokers (N = 10, age: 34.3 ± 13.6) both at rest and during cold pressor test (CPT). Smokers underwent an additional examination after administration of L-Arginine within a median of 7 days of the naïve examination. Results MBF at rest turned out to be 0.77 ± 0.30 (smokers with no L-Arginine; mean ± standard deviation), 0.66 ± 0.21 (smokers L-Arginine) and 0.84 ± 0.08 (nonsmokers). Values under CPT were 1.21 ± 0.42 (smokers no L-Arginine), 1.09 ± 0.35 (smokers L-Arginine) and 1.63 ± 0.33 (nonsmokers). In all groups, MBF was significantly increased under CPT compared to the corresponding rest examination (p < 0.05 in all cases). Additionally, MBF under CPT was significantly different between the smokers and the nonsmokers (p = 0.002). MBF at rest was significantly different between the smokers when L-Arginine was given and the nonsmokers (p = 0.035). Conclusion Short-term smokers showed a reduced response to cold both with and without the administration of L-Arginine. However, absolute MBF values under CPT were lower compared to nonsmokers independently of L-Arginine administration.


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