Promotion of Blood Fluidity Using Electroacupuncture Stimulation

AbstractNeuromuscular electrical stimulation has been used to treat cardiovascular diseases and other types of muscular dysfunction. A novel whole-body neuromuscular electrical stimulation (WB-NMES) wearable device may be beneficial when combined with voluntary exercises. This study aimed to investigate the safety and effects of the WB-NMES on hemodynamics, arrhythmia, and sublingual microcirculation. The study included 19 healthy Japanese volunteers, aged 22–33 years, who were not using any medication. Electrocardiogram (ECG), echocardiography, and blood sampling were conducted before a 20-min WB-NMES session and at 0 and 10 min after termination of WB-NMES. Their tolerable maximum intensity was recorded using numeric rating scale. Arrhythmia was not detected during neuromuscular electrical stimulation or during 10 min of recovery. Blood pressure, heart rate, left ventricular ejection fraction, and diastolic function remained unchanged; however, mild mitral regurgitation was transiently observed during WB-NMES in a single male participant. A decrease in blood glucose and an increase in blood lactate levels were observed, but no changes in blood fluidity, sublingual microcirculation, blood levels of noradrenaline, or oxidative stress were shown. WB-NMES is safe and effective for decreasing blood glucose and increasing blood lactate levels without changing the blood fluidity or microcirculation in healthy people.

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Endothelium as a Source and Target of H2S to Improve Its Trophism and Function

Antioxidants ◽

10.3390/antiox10030486 ◽

2021 ◽

Vol 10 (3) ◽

pp. 486

Author(s):

Valerio Ciccone ◽

Shirley Genah ◽

Lucia Morbidelli

Keyword(s):

Endothelial Dysfunction ◽

Vessel Wall ◽

Redox Reactions ◽

Single Layer ◽

Fine Tuning ◽

Therapeutic Approaches ◽

Impaired Wound Healing ◽

Blood Fluidity ◽

And Function ◽

And Control

The vascular endothelium consists of a single layer of squamous endothelial cells (ECs) lining the inner surface of blood vessels. Nowadays, it is no longer considered as a simple barrier between the blood and vessel wall, but a central hub to control blood flow homeostasis and fulfill tissue metabolic demands by furnishing oxygen and nutrients. The endothelium regulates the proper functioning of vessels and microcirculation, in terms of tone control, blood fluidity, and fine tuning of inflammatory and redox reactions within the vessel wall and in surrounding tissues. This multiplicity of effects is due to the ability of ECs to produce, process, and release key modulators. Among these, gasotransmitters such as nitric oxide (NO) and hydrogen sulfide (H2S) are very active molecules constitutively produced by endotheliocytes for the maintenance and control of vascular physiological functions, while their impairment is responsible for endothelial dysfunction and cardiovascular disorders such as hypertension, atherosclerosis, and impaired wound healing and vascularization due to diabetes, infections, and ischemia. Upregulation of H2S producing enzymes and administration of H2S donors can be considered as innovative therapeutic approaches to improve EC biology and function, to revert endothelial dysfunction or to prevent cardiovascular disease progression. This review will focus on the beneficial autocrine/paracrine properties of H2S on ECs and the state of the art on H2S potentiating drugs and tools.

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Control mechanisms in blood fluidity: role of adenosine triphosphate

Journal of Applied Physiology ◽

10.1152/jappl.1963.18.6.1105 ◽

1963 ◽

Vol 18 (6) ◽

pp. 1105-1110 ◽

Cited By ~ 2

Author(s):

L. O. Pilgeram ◽

D. A. Loegering

Keyword(s):

Energy Metabolism ◽

Adenosine Triphosphate ◽

High Energy ◽

Control Mechanisms ◽

High Energy Phosphate ◽

Cellular Mechanisms ◽

Blood Fluidity ◽

Phosphate Linkage ◽

Glass Surfaces

A possible role for cellular energy metabolism in the control of the blood clotting mechanism has been shown. High-energy phosphate was found to strongly inhibit the recalcification time of plasma prepared with siliconized or glass surfaces. The nucleotide, adenosine triphosphate, in crystalline form and chromatographically pure, will inhibit or completely prevent coagulation in vitro. Reactivity is based primarily on the high-energy phosphate linkage and secondarily upon the nucleoside, adenosine. The principal site of action for ATP is on an unidentified precursor of thromboplastin. Available evidence indicates an important role for energy metabolism in the cellular mechanisms which effect a control over thromboplastin generation and its possible thrombotic and arteriosclerotic sequelae. cellular control mechanisms; blood fluidity; thrombosis arteriosclerosis; aging Submitted on July 1, 1963

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L-cysteine improves blood fluidity impaired by acetaldehyde: In vitro evaluation

PLoS ONE ◽

10.1371/journal.pone.0214585 ◽

2019 ◽

Vol 14 (3) ◽

pp. e0214585 ◽

Cited By ~ 1

Author(s):

Ippo Otoyama ◽

Hironobu Hamada ◽

Tatsushi Kimura ◽

Haruchi Namba ◽

Kiyokazu Sekikawa ◽

...

Keyword(s):

In Vitro Evaluation ◽

Blood Fluidity

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Effects of a hypervolemic hemodilution with HES 100/0.5 10% in patients with PAOD stage II: Elimination kinetics and blood fluidity

Clinical Hemorheology and Microcirculation ◽

10.3233/ch-1996-16506 ◽

1996 ◽

Vol 16 (5) ◽

pp. 631-643

Author(s):

F. Jung ◽

C. Meier ◽

J. Koscielny ◽

G. Pindur ◽

A. Moll ◽

...

Keyword(s):

Stage Ii ◽

Elimination Kinetics ◽

Blood Fluidity ◽

Hypervolemic Hemodilution

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Detection of antitrophoblast antibodies in the sera of patients with anticardiolipin antibodies and fetal loss

Blood ◽

10.1182/blood.v82.9.2730.2730 ◽

1993 ◽

Vol 82 (9) ◽

pp. 2730-2741 ◽

Cited By ~ 35

Author(s):

KR McCrae ◽

AM DeMichele ◽

P Pandhi ◽

MJ Balsai ◽

P Samuels ◽

...

Keyword(s):

Fetal Loss ◽

Thromboxane A2 ◽

First Trimester ◽

Anticardiolipin Antibodies ◽

Trophoblast Cells ◽

Fetal Demise ◽

Blood Fluidity ◽

Increased Risk ◽

History Of ◽

Placental Blood

Abstract Women with anticardiolipin antibodies (ACLA) are at increased risk for fetal loss. One potential explanation for this outcome is that sera from these individuals contain antibodies reactive with trophoblast cells, which are involved in the establishment of the uteroplacental vasculature and maintenance of placental blood fluidity. To examine this hypothesis, we compared the incidence of trophoblast-reactive antibodies in 27 patients with ACLA and a history of fetal loss with that in 29 normal pregnant women. Sera from 20 patients, but only one control, contained trophoblast-reactive antibodies (P < .001). These antibodies were not directed against major histocompatibility class I antigens, and reacted with both term and first-trimester trophoblast cells. In most cases, sera from which ACLA were adsorbed by cardiolipin- containing liposomes maintained reactivity against cells. In addition, patient Ig fractions immunoprecipitated an approximately 62-kD protein from the trophoblast cell surface, stimulated the release of arachidonic acid and thromboxane A2 by trophoblasts, and inhibited the binding of prourokinase to trophoblast urokinase receptors. These observations show that sera from women with ACLA and a history of fetal loss contain antitrophoblast antibodies. These antibodies may be serologically distinct from ACLA, and may contribute to the pathogenesis of fetal demise.

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