scholarly journals Doppler Mitral Inflow Variables Time Course After Treadmill Stress Echo with and Without Ischemic Response

Author(s):  
FABIJAN LULIĆ ◽  
ZDRAVKO VIRAG

Abstract This study evaluated Doppler mitral inflow variables changes from rest to post-exercise among 104 subjects with and without echocardiographic evidence of ischemic response (IR) to exercise (63.9 ± 11 years, 54% male, 32% with IR) who underwent a clinically indicated treadmill stress echo (TSE) test. The time from exercise cessation to imaging (TIME) was recorded. The changes (after TSE minus baseline values) in the peak E-wave velocity (∆E) [34.2 vs. 24.2, p = 0.024] and E-wave deceleration rate (∆DR) [348.0 vs. 225.7, p = 0.010] were bigger in ischemic than in nonischemic subjects, while the changes in the peak A-wave velocity (∆A) did not differ [7.9 vs. 15.0, p = 0.082]. The correlations between Doppler variables and IR, TIME, and TIME*IR interaction were analyzed. We observed a significant interaction between TIME and IR regarding ∆E and ∆DR. The differences in the regression line slopes of time courses for ∆E and ∆DR based on IR were significant: ∆E (–0.09 vs. –8.17, p = 0.037) and ∆DR (11.23 vs. –82.60, p = 0.022). Main findings: 1. Time courses after exercise of ∆E and ∆DR in subjects with and without IR were different. 2. ∆E and ∆DR did not differ between subjects with and without IR at exercise cessation (TIME = 0). 3. The simple main effect of ischemia on ∆E and ∆DR was significant at TIME of ≥3 min. Divergent time courses of ∆E and ∆DR after exercise might be promising for detecting diastolic dysfunction caused by ischemia.

Author(s):  
Gabriel Kolesny Tricot ◽  
Fabiula Isoton Isoton Novelli ◽  
Lucieli Teresa Cambri

AbstractThis study aimed to assess whether obesity and/or maximal exercise can change 24 h cardiac autonomic modulation and blood pressure in young men. Thirty-nine men (n: 20; 21.9±1.8 kg·m−2, and n: 19; 32.9±2.4 kg·m−2) were randomly assigned to perform a control (non-exercise) and an experimental day exercise (after maximal incremental test). Cardiac autonomic modulation was evaluated through frequency domain heart rate variability (HRV). Obesity did not impair the ambulatory HRV (p>0.05), however higher diastolic blood pressure during asleep time (p=0.02; group main effect) was observed. The 24 h and awake heart rate was higher on the experimental day (p<0.05; day main effect), regardless of obesity. Hypotension on the experimental day, compared to control day, was observed (p<0.05). Obesity indicators were significantly correlated with heart rate during asleep time (Rho=0.34 to 0.36) and with ambulatory blood pressure(r/Rho=0.32 to 0.53). Furthermore, the HRV threshold workload was significantly correlated with ambulatory heart rate (r/Rho=− 0.38 to−0.52). Finally, ambulatory HRV in obese young men was preserved; however, diastolic blood pressure was increased during asleep time. Maximal exercise caused heart rate increase and 24h hypotension, with decreased cardiac autonomic modulation in the first hour, regardless of obesity.


Author(s):  
Garrett C. Jones ◽  
Jonathan D. Blotter ◽  
Cameron D. Smallwood ◽  
Dennis L. Eggett ◽  
Darryl J. Cochrane ◽  
...  

This study utilized resonant frequency vibration to the upper body to determine changes in pain, stiffness and isometric strength of the biceps brachii after eccentric damage. Thirty-one participants without recent resistance training were randomized into three groups: a Control (C) group and two eccentric exercise groups (No vibration (NV) and Vibration (V)). After muscle damage, participants in the V group received upper body vibration (UBV) therapy for 5 min on days 1–4. All participants completed a visual analog scale (VAS), maximum voluntary isometric contraction (MVIC), and shear wave elastography (SWE) of the bicep at baseline (pre-exercise), 24 h, 48 h, and 1-week post exercise. There was a significant difference between V and NV at 24 h for VAS (p = 0.0051), at 24 h and 1-week for MVIC (p = 0.0017 and p = 0.0016, respectively). There was a significant decrease in SWE for the V group from 24–48 h (p = 0.0003), while there was no significant change in the NV group (p = 0.9341). The use of UBV resonant vibration decreased MVIC decrement and reduced VAS pain ratings at 24 h post eccentric damage. SWE was strongly negatively correlated with MVIC and may function as a predictor of intrinsic muscle state in the time course of recovery of the biceps brachii.


1992 ◽  
Vol 99 (3) ◽  
pp. 317-338 ◽  
Author(s):  
L Reuss ◽  
B Simon ◽  
C U Cotton

The mechanisms of apparent streaming potentials elicited across Necturus gallbladder epithelium by addition or removal of sucrose from the apical bathing solution were studied by assessing the time courses of: (a) the change in transepithelial voltage (Vms). (b) the change in osmolality at the cell surface (estimated with a tetrabutylammonium [TBA+]-selective microelectrode, using TBA+ as a tracer for sucrose), and (c) the change in cell impermeant solute concentration ([TMA+]i, measured with an intracellular double-barrel TMA(+)-selective microelectrode after loading the cells with TMA+ by transient permeabilization with nystatin). For both sucrose addition and removal, the time courses of Vms were the same as the time courses of the voltage signals produced by [TMA+]i, while the time courses of the voltage signals produced by [TBA+]o were much faster. These results suggest that the apparent streaming potentials are caused by changes of [NaCl] in the lateral intercellular spaces, whose time course reflects the changes in cell water volume (and osmolality) elicited by the alterations in apical solution osmolality. Changes in cell osmolality are slow relative to those of the apical solution osmolality, whereas lateral space osmolality follows cell osmolality rapidly, due to the large surface area of lateral membranes and the small volume of the spaces. Analysis of a simple mathematical model of the epithelium yields an apical membrane Lp in good agreement with previous measurements and suggests that elevations of the apical solution osmolality elicit rapid reductions in junctional ionic selectivity, also in good agreement with experimental determinations. Elevations in apical solution [NaCl] cause biphasic transepithelial voltage changes: a rapid negative Vms change of similar time course to that of a Na+/TBA+ bi-ionic potential and a slow positive Vms change of similar time course to that of the sucrose-induced apparent streaming potential. We conclude that the Vms changes elicited by addition of impermeant solute to the apical bathing solution are pseudo-streaming potentials, i.e., junctional diffusion potentials caused by salt concentration changes in the lateral intercellular spaces secondary to osmotic water flow from the cells to the apical bathing solution and from the lateral intercellular spaces to the cells. Our results do not support the notion of junctional solute-solvent coupling during transepithelial osmotic water flow.


1991 ◽  
Vol 97 (2) ◽  
pp. 303-320 ◽  
Author(s):  
A Castellano ◽  
J López-Barneo

Voltage-gated Na+ and Ca2+ conductances of freshly dissociated septal neurons were studied in the whole-cell configuration of the patch-clamp technique. All cells exhibited a large Na+ current with characteristic fast activation and inactivation time courses. Half-time to peak current at -20 mV was 0.44 +/- 0.18 ms and maximal activation of Na+ conductance occurred at 0 mV or more positive membrane potentials. The average value was 91 +/- 32 nS (approximately 11 mS cm-2). At all membrane voltages inactivation was well fitted by a single exponential that had a time constant of 0.44 +/- 0.09 ms at 0 mV. Recovery from inactivation was complete in approximately 900 ms at -80 mV but in only 50 ms at -120 mV. The decay of Na+ tail currents had a single time constant that at -80 mV was faster than 100 microseconds. Depolarization of septal neurons also elicited a Ca2+ current that peaked in approximately 6-8 ms. Maximal peak Ca2+ current was obtained at 20 mV, and with 10 mM external Ca2+ the amplitude was 0.35 +/- 0.22 nA. During a maintained depolarization this current partially inactivated in the course of 200-300 ms. The Ca2+ current was due to the activity of two types of conductances with different deactivation kinetics. At -80 mV the closing time constants of slow (SD) and fast (FD) deactivating channels were, respectively, 1.99 +/- 0.2 and 0.11 +/- 0.03 ms (25 degrees C). The two kinds of channels also differed in their activation voltage, inactivation time course, slope of the conductance-voltage curve, and resistance to intracellular dialysis. The proportion of SD and FD channels varied from cell to cell, which may explain the differential electrophysiological responses of intracellularly recorded septal neurons.


1980 ◽  
Vol 152 (5) ◽  
pp. 1302-1310 ◽  
Author(s):  
D S Pisetsky ◽  
G A McCarty ◽  
D V Peters

The quantitative expression of anti-DNA and anti-Sm antibodies has been investigated in autoimmune MRL-lpr/lpr and MRL-+/+ mice. Anti-Sm antibodies were detected in sera from 21/23 lpr/lpr and 10/16 +/+ mice, with individual animals showing striking variation in the time-course and magnitude of this autoantibody response. The peak antibody levels of the responding animals of each substrain did not differ significantly. For anti-DNA antibody, a different pattern of responsiveness was observed. Individual animals of each substrain produced very similar responses in terms of the magnitude and time-course of serum anti-DNA antibody. The differences in the peak levels of the two substrains were highly significant, with lpr/lpr mice demonstrating a much greater anti-DNA antibody response than +/+ mice. In lpr/lpr mice tested for both autoantibody systems, serum anti-DNA and anti-Sm antibodies showed distinct time-courses. These studies indicate that anti-DNA and anti-Sm antibodies are expressed independently in MRL mice, with the expression of anti-DNA, but not anti-Sm antibody markedly influenced by the presence of the 1pr gene. A fundamental difference in the mechanisms involved in the generation of anti-DNA and anti-Sm antibodies is suggested by the quantitative pattern of the two responses.


2015 ◽  
Vol 146 (1) ◽  
pp. 15-36 ◽  
Author(s):  
Giovanni Gonzalez-Gutierrez ◽  
Claudio Grosman

The superfamily of pentameric ligand-gated ion channels (pLGICs) is unique among ionotropic receptors in that the same overall structure has evolved to generate multiple members with different combinations of agonist specificities and permeant-ion charge selectivities. However, aside from these differences, pLGICs have been typically regarded as having several invariant functional properties. These include pore blockade by extracellular quaternary-ammonium cations in the micromolar-to-millimolar concentration range (in the case of the cation-selective members), and a gain-of-function phenotype, which manifests as a slower deactivation time course, as a result of mutations that reduce the hydrophobicity of the transmembrane pore lining. Here, we tested this notion on three distantly related cation-selective members of the pLGIC superfamily: the mouse muscle nicotinic acetylcholine receptor (nAChR), and the bacterial GLIC and ELIC channels. Remarkably, we found that, whereas low millimolar concentrations of TMA+ and TEA+ block the nAChR and GLIC, neither of these two quaternary-ammonium cations blocks ELIC at such concentrations; instead, both carry measurable inward currents when present as the only cations on the extracellular side. Also, we found that, whereas lidocaine binding speeds up the current-decay time courses of the nAChR and GLIC in the presence of saturating concentrations of agonists, the binding of lidocaine to ELIC slows this time course down. Furthermore, whereas mutations that reduce the hydrophobicity of the side chains at position 9′ of the M2 α-helices greatly slowed the deactivation time course of the nAChR and GLIC, these mutations had little effect—or even sped up deactivation—when engineered in ELIC. Our data indicate that caution should be exercised when generalizing results obtained with ELIC to the rest of the pLGICs, but more intriguingly, they hint at the possibility that ELIC is a representative of a novel branch of the superfamily with markedly divergent pore properties despite a well-conserved three-dimensional architecture.


2014 ◽  
Vol 5 ◽  
pp. JCM.S13738 ◽  
Author(s):  
Satoru Sakuma ◽  
Daisuke Tokuhara ◽  
Hiroshi Otsubo ◽  
Tsunekazu Yamano ◽  
Haruo Shintaku

Background The time course of cytokine dynamics after seizure remains controversial. Here we evaluated the changes in the levels and sites of interleukin (IL)-1β expression over time in the hippocampus after seizure. Methods Status epilepticus (SE) was induced in adult Wistar rats by means of intraperitoneal injection of kainic acid (KA). Subsequently, the time courses of cellular localization and IL-1β concentration in the hippocampus were evaluated by means of immunohistochemical and quantitative assays. Results On day 1 after SE, CA3 pyramidal cells showed degeneration and increased IL-1β expression. In the chronic phase (>7 days after SE), glial fibrillary acidic protein (GFAP)–-positive reactive astrocytes–-appeared in CA1 and became IL-1β immunoreactive. Their IL-1β immunoreactivity increased in proportion to the progressive hypertrophy of astrocytes that led to gliosis. Quantitative analysis showed that hippocampal IL-1β concentration progressively increased during the acute and chronic phases. Conclusion IL-1β affects the hippocampus after SE. In the acute phase, the main cells expressing IL-1β were CA3 pyramidal cells. In the chronic phase, the main cells expressing IL-1β were reactive astrocytes in CA1.


2012 ◽  
Vol 7 ◽  
Author(s):  
Roberto W. Dal Negro ◽  
Silvia Tognella ◽  
Luca Bonadiman ◽  
Paola Turco

Background: Information on the effects of long-term oxygen treatment (LTOT) on blood hemoglobin (Hb) in severe COPD are limited. The aim was to assess blood Hb values in severe COPD, and investigate the time-course of both Hb and blood gas changes during a 3-year telemetric LTOT. Methods: A cohort of 132 severe COPD patients (94 males; 71.4 years ± 8.8 sd), newly admitted to the tele-LTOT program, was investigated. Subjects were divided according to their original blood Hb: group A: <13 g/dL; group B: ≥13<15 g/dL; group C: ≥ 5<16 g/dL; group D: ≥16 g/dL. Blood Hb (g/dL), PaO2 and PaCO2 (mmHg), SaO2 (%), and BMI were measured at LTOT admission (t0), and at least quarterly over three years (t1-t3). Wilcoxon test was used to compare t0 vs. t1 values; linear regression to assess a possible Hb-BMI relationship; ANOVA to compare changes in Hb time-courses over the 3 years. Results: LTOT induced a systematic increase of PaO2, and changes were significant since the first year (from 52.1 mmHg± 6.6sd to 65.1 mmHg± 8.7 sd, p<0.001). Changes in SaO2 were quite similar. Comparable and equally significant trends were seen in all subgroups (p<0.001). PaCO2 dropped within the first year of LTOT (from 49.4 mmHg± 9.1sd to 45.9 mmHg ±7.5 sd, p<0.001): the t0-t1 comparison proved significant (p<0.01) only in subgroups with the highest basal Hb, who showed a further PaCO2 decline over the remaining two years (p<0.001). Hb tended to normalization during LTOT only in subgroups with basal Hb>15 g/dl (ANOVA p<0.001); anemic subjects (Hb<13 g/dl) ameliorated not significantly in the same period (ANOVA = 0.5). Survival was independent of the original blood Hb. Anemia and polyglobulia are differently prevalent in COPD, the latter being the most represented in our cohort. LTOT affected both conditions, but to a different extent and according to different time-courses. The most striking Hb improvement was in polyglobulic patients in whom also PaO2, PaCO2 and SaO2 dramatically improved. In anemic subjects effects were smaller and slower, oxygenation being equally ameliorated by LTOT. Conclusions: LTOT effects on Hb and PaCO2 are regulated by an Hb-dependent gradient which seems independent of the original impairment of blood gases and of effects on oxygenation.


2021 ◽  
Vol 11 (18) ◽  
pp. 8783
Author(s):  
Hsin-Fu Lin ◽  
Yi-Hung Liao ◽  
Pai-Chi Li

Purpose: this study investigated the effects of the intensity of machine-based bicep curl resistance exercise on ultrafast ultrasound-derived muscle strain rate and carotid ultrafast pulse wave velocity (ufPWV), and examined the association between muscle strain rate, ufPWV, and established carotid function measures in habitual resistance-trained individuals. Methods: twenty-three young habitual resistance-trained males (age: 24 ± 1 year, body mass index = 24 ± 1 kg/m2) were recruited to participate in two bouts of acute bicep curl exercise. After one-repetition maximum determination (1RM), the participants were randomly assigned to engage in bicep curls at 40 or 80%1RM intensity (10 reps × five sets) by a crossover study design. The muscle strain rate of bicep muscle, carotid ufPWV during systole(ufPWV-sys), and diastole (ufPWV-dia) were obtained pre- and post-exercise. In addition, carotid function measures were calculated by obtained carotid diameter and central blood pressure changes. Results: compared with pre-exercise, the reduction in post-exercise muscle strain rate and its area under the curve of 80%1RM was greater than those of 40%1RM. Both ufPWV-sys and ufPWV-dia increased regardless of exercise intensity. Baseline bicep muscle strain rate correlated not only with ufPWV-sys (r = −0.71, p = 0.001), ufPWV-dia (r = −0.74, p = 0.001), but also carotid compliance (r = 0.49, p = 0.02), distensibility (r = 0.54, p = 0.01) and ß stiffness (r= −0.84, p < 0.0001). The ufPWVs also correlated with ß stiffness (r = 0.64–0.76, p = 0.01). Conclusion: muscle stiffness measured by ultrafast ultrasound elastography increases positively with resistance exercise intensity, and it appears to correlate with carotid ufPWV and established carotid function measures in habitual resistance-trained individuals.


1977 ◽  
Vol 69 (1) ◽  
pp. 173-185
Author(s):  
C. M. Wood ◽  
B. R. McMahon ◽  
D. G. McDonald

Exhausting activity results in a marked and immediate drop in blood pH which gradually returns to normal over the following 6h. The acidosis is caused largely by elevated Pco2 levels, which vary inversely with pH. Blood lactate concentration increases slowly, reaching a maximum at 2--4h post-exercise, and contributes significantly to the acidosis only late in the recovery period. The slow time course of lactic acid release into the blood permits temporal separation of the peak metabolic acidosis from the peak respiratory acidosis. Evidence is presented that a metabolic acid other than lactic also makes a modest contribution to the pH depression during the recovery period.


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