Cardiac function during mental stress: cholinergic modulation with pyridostigmine in healthy subjects

2003 ◽  
Vol 105 (2) ◽  
pp. 161-165 ◽  
Author(s):  
Isis Délio SANT'ANNA ◽  
Eduardo Branco DE SOUSA ◽  
Alvaro Villela DE MORAES ◽  
Débora Lopes LOURES ◽  
Evandro Tinoco MESQUITA ◽  
...  
Keyword(s):  
Oral Administration ◽  
Mental Stress ◽  
Healthy Subjects ◽  
Mental Arithmetic ◽  
Systolic Pressure ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Stress Tests ◽  
Mean Velocity ◽  
Double Blind

Mentally or emotionally stressful situations occur throughout our lives and cause physiological haemodynamic responses. In patients with coronary artery disease, such events can also induce myocardial ischaemia and ventricular arrhythmias, increasing mortality rates. The purpose of the present study was to determine the acute effects of the oral administration of pyridostigmine, a reversible cholinesterase inhibitor and thus an indirect cholinomimetic drug, on echocardiographic variables during mental stress in healthy subjects. A total of 18 healthy young volunteers were subjected to mental stress tests (mental arithmetic and the Stroop colour–word test) 2 h after the oral administration of either placebo or pyridostigmine bromide (45 mg), using a balanced-randomized, double-blind, crossover protocol. During mental stress, heart rate (pyridostigmine, 64±1 beats/min; placebo, 70±1 beats/min; P=0.0003) and diastolic blood pressure (pyridostigmine, 66±2 mmHg; placebo, 79±3 mmHg; P=0.01) were lower in the pyridostigmine group, but systolic pressure was not (pyridostigmine, 124±3 mmHg; placebo, 123±3 mmHg; P=0.40). There were no detectable abnormalities in the left ventricular wall motion score during mental stress, but left ventricular outflow tract mean velocity (pyridostigmine, 0.68±0.02 m/s; placebo, 0.64±0.02 m/s; P<0.05) and mitral inflow velocity deceleration (placebo, 4.05±0.18 m/s2; pyridostigmine, 4.41±0.16 m/s2; P<0.05) were higher in the pyridostigmine group. In conclusion, cholinergic stimulation with pyridostigmine seems to increase left ventricular diastolic function during mental stress in healthy subjects.

Cardiovascular reactivity in isometric exercise and mental arithmetic in children

1994 ◽  
Vol 76 (1) ◽  
pp. 146-150 ◽  
Author(s):  
H. A. Verhaaren ◽  
R. M. Schieken ◽  
P. Schwartz ◽  
M. Mosteller ◽  
D. Matthys ◽  
...  
Keyword(s):  
Cardiovascular Reactivity ◽  
Stress Responses ◽  
Mental Stress ◽  
Mental Arithmetic ◽  
Isometric Exercise ◽  
Left Ventricular ◽  
Stress Tests ◽  
Isometric Handgrip ◽  
Cardiovascular Stress ◽  
Changes Over Time

In children, we studied noninvasively the cardiovascular stress responses, including changes over time of systolic blood pressure (SBP), heart rate (HR), and stroke volume (SV) in isometric handgrip (IHG) and mental arithmetic. Specifically, we asked whether 1) these cardiovascular stress responses were different for the two stress conditions in children, 2) these responses differed in boys and girls, and 3) the anthropometric variables related to these stress responses. SV differed significantly between IHG and mental arithmetic over the entire stress period. This may reflect higher systemic vascular resistance during IHG. HR in boys was lower than in girls over the entire period of stress in both stress tests. This observation cannot be attributed to differences in conditioning, because this should not influence responses to isometric or mental stress. A larger left ventricular mass was related to higher SVs. A marked relationship was found between HR and SBP and between HR and SV. No relationship was found between SBP and SV.

Role of Diastole in Left Ventricular Function, I: Biochemical and Biomechanical Events

2004 ◽  
Vol 13 (5) ◽  
pp. 394-403 ◽  
Author(s):  
Penelope S. Villars ◽  
Shannan K. Hamlin ◽  
Andrew D. Shaw ◽  
Joseph T. Kanusky
Keyword(s):  
Left Ventricle ◽  
Calcium Release ◽  
Troponin I ◽  
Regulatory Protein ◽  
Systolic Pressure ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Release Mechanism ◽  
Adrenergic Stimulation ◽  
Inotropic State

Left ventricular diastolic function plays an important role in cardiac physiology. Lusitropy, the ability of the cardiac myocytes to relax, is affected by both biochemical events within the myocyte and biomechanical events in the left ventricle. β-Adrenergic stimulation alters diastole by enhancing the phosphorylation of phospholamban, a substrate within the myocyte that increases the uptake of calcium ions into the sarcoplasmic reticulum, increasing the rate of relaxation. Troponin I, a regulatory protein involved in the coupling of excitation to contraction, is vital to maintaining the diastolic state; depletion of troponin I can produce diastolic dysfunction. Other biochemical events, such as defects in the voltage-sensitive release mechanism or in inositol triphosphate calcium release channels, have also been implicated in altering diastolic tone. Extracellular collagen determines myocardial stiffness; impaired glucose tolerance can induce an increase in collagen cross-linking and lead to higher end-diastolic pressures. The passive properties of the left ventricle are most accurately measured during the diastasis and atrial contraction phases of diastole. These phases of the cardiac cycle are the least affected by volume status, afterload, inherent viscoelasticity, and the inotropic state of the myocardium. Diastolic abnormalities can be conceptualized by using pressure-volume loops that illustrate myocardial work and both diastolic and systolic pressure-volume relationships. The pressure-volume model is an educational tool that can be used to demonstrate isolated changes in preload, afterload, inotropy, and lusitropy and their interaction.

Electrophysiological effects of transient aortic occlusion in intact canine heart

1985 ◽  
Vol 249 (5) ◽  
pp. H1017-H1023 ◽  
Author(s):  
D. G. Benditt ◽  
J. M. Kriett ◽  
H. G. Tobler ◽  
C. C. Gornick ◽  
B. L. Detloff ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Drive Train ◽  
Aortic Occlusion ◽  
Canine Heart ◽  
Stroke Work ◽  
Shortening Velocity ◽  
Mean Velocity ◽  
Transient Aortic Occlusion ◽  
Premature Beats

This study utilized sonomicrometers transmural multipolar electrodes and cardiac electrical stimulation techniques to examine the effect on myocardial electrophysiological characteristics of altering ventricular systolic mechanical properties by transient aortic occlusion. Nine anesthetized open-chest dogs were atrially paced, and timed extrastimuli were inserted during alternate drive-train sequences at right or left ventricular (RV, LV) epicardial sites to measure ventricular effective refractory period (ERP). Sonomicrometer measurements of LV systolic mechanical parameters and both RV and LV electrophysiological findings were determined prior to and during periods of transient aortic occlusion. Aortic occlusion was applied just prior to the last beat of each eight-beat atrial drive train and released immediately following the programmed ventricular extrastimulus. Aortic occlusion increased LV systolic pressure (+42 +/- 26.6 mmHg, P less than 0.01) and diminished segmental stroke shortening (0.100 +/- 0.059 mm, P less than 0.02), shortening fraction (0.086 +/- 0.048, P less than 0.001), mean velocity of stroke shortening (0.444 +/- 0.186 mm/s, P less than 0.001), and stroke work (P less than 0.001). LV epicardial and endocardial ERP were prolonged as a result of aortic occlusion (5 +/- 7.2 and 6 +/- 6.5 ms, respectively, P less than 0.05), whereas RV ERP was unchanged. Latency of premature beats at equivalent coupling intervals was unaltered. ERP prolongation correlated most strongly with reductions of segmental stroke shortening (r = 0.928, P less than 0.001), shortening fraction (r = 0.901, P less than 0.001), and mean shortening velocity (r = 0.819, P less than 0.01). Thus transient aortic occlusion prolonged LV refractoriness, and electrophysiological changes closely paralleled the severity of systolic mechanical disturbance.

scholarly journals Melatonin attenuates the skin sympathetic nerve response to mental stress

2013 ◽  
Vol 305 (9) ◽  
pp. H1382-H1386 ◽  
Author(s):  
Matthew D. Muller ◽  
Charity L. Sauder ◽  
Chester A. Ray
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Mental Stress ◽  
Sympathetic Nerve Activity ◽  
Mental Arithmetic ◽  
Experimental Testing ◽  
Double Blind ◽  
Before And After ◽  
The Mean

Melatonin attenuates muscle sympathetic nerve responses to sympathoexcitatory stimuli, but it is unknown whether melatonin similarly attenuates reflex changes in skin sympathetic nerve activity (SSNA). In this double-blind, placebo-controlled, crossover study, we tested the hypothesis that melatonin (3 mg) would attenuate the SSNA response to mental stress (mental arithmetic). Twelve healthy subjects underwent experimental testing on two separate days. Three minutes of mental stress occurred before and 45 min after ingestion of melatonin (3 mg) or placebo. Skin temperature was maintained at 34°C. Reflex increases in SSNA (peroneal nerve), mean arterial pressure, and heart rate (HR) to mental stress before and after melatonin were determined. Melatonin lowered HR (pre, 66 ± 3 beats/min; and post, 62 ± 3 beats/min, P = 0.046) and SSNA (pre, 14,282 ± 3,706 arbitrary units; and post, 9,571 ± 2,609 arbitrary units, P = 0.034) at rest. In response to mental stress, SSNA increases were significantly attenuated following melatonin ingestion (second minute, 114 ± 30 vs. 74 ± 14%; and third minute, 111 ± 29 vs. 54 ± 12%, both P < 0.05). The mean arterial pressure increase to mental stress was blunted in the third minute (20 ± 2 vs. 17 ± 2 mmHg, P = 0.032), and the HR increase was blunted in the first minute (33 ± 3 vs. 29 ± 3 beats/min, P = 0.034) after melatonin. In summary, exogenous melatonin attenuates the SSNA response to mental stress.

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