Platelets Do Not Alter Flow-Mediated Dilation or Arterial Conduction in vivo

2021 ◽  
pp. 1-6
Author(s):  
Therese Ruane-O’Hora ◽  
Farouk Markos
Keyword(s):  
Shear Stress ◽  
Platelet Count ◽  
Platelet Rich Plasma ◽  
Flow Mediated Dilation ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Vascular Bed ◽  
Before And After

The aim of this study was to investigate whether platelets contribute to shear stress and vascular conductance in the iliac vascular bed in vivo. Flow-mediated dilation of pig iliac was induced by downstream injection of acetylcholine (50 μg), and separately, conductance (ΔF/ΔP) was calculated. This was carried out before and after removal of 1 L of arterial blood in 240 mL increments, and each 240 mL was spun in a centrifuge (1,500 rcf for 7 min); platelet-rich plasma was replaced with equal volume of heparinised saline and reinjected. The circulating platelet count fell from 369 × 10<sup>9</sup>/L (<i>n</i> = 5) to 165 × 10<sup>9</sup>/L (<i>p</i> = 0.01; <i>n</i> = 4; Student’s unpaired <i>t</i>). An increase in flow led to an increase in the iliac diameter by 0.49 ± 0.03 mm (mean ± SEM) before platelet reduction and 0.55 ± 0.05 mm after (<i>p</i> = 0.36, Student’s paired <i>t</i>, <i>n</i> = 5); the change in arterial conductance was also not significantly affected by platelet reduction, control: 1.44 ± 0.34 mL/min/mm Hg, after platelet reduction: 1.39 ± 0.04 mm (<i>p</i> = 0.55, Student’s paired <i>t</i>, <i>n</i> = 4). Therefore, platelets do not contribute to shear stress or conductance in vivo.

Heparan sulphate and hyaluronic acid components of the glycocalyx do not play a role in flow-mediated dilation of the iliac in the anaesthetized pig

2019 ◽  
Vol 97 (8) ◽  
pp. 746-752
Author(s):  
T. Ruane-O’Hora ◽  
D. O’Malley ◽  
M.M. Buckley ◽  
F. Markos
Keyword(s):  
Shear Stress ◽  
Hyaluronic Acid ◽  
Heparan Sulphate ◽  
Flow Mediated Dilation ◽  
Similar Increase ◽  
Shear Stress Sensor ◽  
Before And After ◽  
Student’S T ◽  
Student’S T Test

The shear-stress sensor function of vascular glycocalyx heparan sulphate and hyaluronic acid was investigated in vivo by assessing flow-mediated dilation before and after their removal. Heparinase III exposure (100 mU·mL−1 for 20 min;n = 6) did not significantly affect flow-mediated dilation of the iliac, from 0.42 ± 0.08 mm (mean ± SEM) to 0.34 ± 0.07 mm after (P = 0.12; paired Student’s t test) for a statistically similar increase in shear stress; 18.24 ± 4.2 N·m−2 for the control and 15.8 ± 3.6 N·m−2 for the heparinase III experiment (P = 0.18). Hyaluronidase exposure (0.14–1.4 mg·mL−1 for 20 min; n = 8) also did not significantly reduce flow-mediated dilation of the iliac, which averaged 0.39 ± 0.08 mm before and 0.38 ± 0.09 mm after (P = 0.11) for a statistically similar increase in shear stress; 11.90 ± 3.20 N·m−2 for the control and 9.8 ± 3.33 N·m−2 for the hyaluronidase experiment (P = 0.88). Removal of both heparan sulphate and hyaluronic acid was confirmed using immunohistochemistry. Neither the heparan sulphate nor the hyaluronic acid components of the glycocalyx mediate shear-stress-induced vasodilation in conduit arteries in vivo.

Enhancement of ADP-induced Platelet Aggregation by Adrenaline in Vivo and Its Prevention

1973 ◽  
Vol 29 (02) ◽  
pp. 490-498 ◽  
Author(s):  
Hiroh Yamazaki ◽  
Itsuro Kobayashi ◽  
Tadahiro Sano ◽  
Takio Shimamoto
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
The Other ◽  
Endothelial Surface ◽  
Important Interaction ◽  
Blood Coagulability ◽  
The Difference

SummaryThe authors previously reported a transient decrease in adhesive platelet count and an enhancement of blood coagulability after administration of a small amount of adrenaline (0.1-1 µg per Kg, i. v.) in man and rabbit. In such circumstances, the sensitivity of platelets to aggregation induced by ADP was studied by an optical density method. Five minutes after i. v. injection of 1 µg per Kg of adrenaline in 10 rabbits, intensity of platelet aggregation increased to 115.1 ± 4.9% (mean ± S. E.) by 10∼5 molar, 121.8 ± 7.8% by 3 × 10-6 molar and 129.4 ± 12.8% of the value before the injection by 10”6 molar ADP. The difference was statistically significant (P<0.01-0.05). The above change was not observed in each group of rabbits injected with saline, 1 µg per Kg of 1-noradrenaline or 0.1 and 10 µg per Kg of adrenaline. Also, it was prevented by oral administration of 10 mg per Kg of phenoxybenzamine or propranolol or aspirin or pyridinolcarbamate 3 hours before the challenge. On the other hand, the enhancement of ADP-induced platelet aggregation was not observed in vitro, when 10-5 or 3 × 10-6 molar and 129.4 ± 12.8% of the value before 10∼6 molar ADP was added to citrated platelet rich plasma (CPRP) of rabbit after incubation at 37°C for 30 second with 0.01, 0.1, 1, 10 or 100 µg per ml of adrenaline or noradrenaline. These results suggest an important interaction between endothelial surface and platelets in connection with the enhancement of ADP-induced platelet aggregation by adrenaline in vivo.

Tracings of Behavior of Myoblasts Cultured Under Couette Type of Shear Flow Between Parallel Disks

2021 ◽  
Author(s):  
Shigehiro Hashimoto ◽  
Hiroki Yonezawa
Keyword(s):  
Shear Stress ◽  
Shear Flow ◽  
Rotating Disk ◽  
Time Lapse ◽  
Mechanical Stimuli ◽  
Parallel Disks ◽  
Before And After ◽  
A Cell

Abstract A cell deforms and migrates on the scaffold under mechanical stimuli in vivo. In this study, a cell with division during shear stress stimulation has been observed in vitro. Before and after division, both migration and deformation of each cell were analyzed. To make a Couette-type shear flow, the medium was sandwiched between parallel disks (the lower stationary culture-disc and the upper rotating disk) with a constant gap. The wall shear stress (1.5 Pa &lt; τ &lt; 2 Pa) on the surface of the lower culture plate was controlled by the rotational speed of the upper disc. Myoblasts (C2C12: mouse myoblast cell line) were used in the test. After cultivation without flow for 24 hours for adhesion of the cells to the lower disk, constant τ was applied to the cells in the incubator for 7 days. The behavior of each cell during shear was tracked by time-lapse images observed by an inverted phase contrast microscope placed in the incubator. Experimental results show that each cell tends to divide after higher activities: deformation and migration. The tendency is remarkable at the shear stress of 1.5 Pa.

Slow postcapillary pH changes in blood in anesthetized animals

1978 ◽  
Vol 45 (5) ◽  
pp. 674-680 ◽  
Author(s):  
A. Bidani ◽  
E. D. Crandall
Keyword(s):  
Blood Cells ◽  
Ph Change ◽  
Arterial Blood ◽  
Blood Ph ◽  
Pulmonary Capillary ◽  
Before And After ◽  
Equilibration Process ◽  
Contact Surfaces ◽  
Electrode Chamber

To investigate the hypothesis that blood pH and PCO2 continue to change after the blood leaves an exchange capillary, we used a rapidly responding, pressure-insensitive, stopped-flow pH electrode apparatus. Arterial blood from an anesthetized dog or cat is drawn through the apparatus into a syringe. Syringe movement is then suddenly stopped. Temperature and pH of the blood in the electrode assembly are continuously monitored, both before and after blood withdrawal ceases. Hemolysis was reduced by coating all blood contact surfaces with silicone and fasting the animal overnight, anesthetizing it with crystalline pentobarbital sodium, and allowing it to ventilate spontaneously. After stopping withdrawal, pH of blood in the electrode chamber continued to change, rising 0.01 unit with t1/2 of 4.4 s. After lysed blood was returned to the animal to provide carbonic anhydrase to the plasma, no pH change was seen after stopping the flow. The small pH rise occurring in arterial blood in vivo is probably due in large part to disequilibrium of [H+] between red blood cells and plasma at the end of the pulmonary capillary, the equilibration process being rate-limited by the extracellular CO2 hydration-dehydration reaction.

scholarly journals Decrease in Platelet Aggregability after Total Oophorectomy

1977 ◽  
Author(s):  
H. Yamazaki ◽  
T. Motomiya ◽  
M. Sonoda ◽  
N. Miyagawa
Keyword(s):  
Platelet Count ◽  
Clinical Evidence ◽  
Coulter Counter ◽  
Control Group ◽  
Bilateral Oophorectomy ◽  
Platelet Volume ◽  
Platelet Aggregability ◽  
Significant Difference ◽  
Before And After

Substantial clinical evidence indicates that large doses of estrogen frequenly result in thromboembolic disorders. Effects of estrogen on platelet aggregability were examined in women with uterine myoma before and after oophorectomy. Bilateral oophorectomy on 15 cases (48.7+0.12 yrs, mean+SE) and unilateral or no oophorectomy on 18 cases (control group : 42.2+0.18 yrs) were performed with myomectomy of the uterus. On one day before and one day, one week and one month after the operation performed, their platelet count by Coulter counter, platelet volume by Coulter channelyzer and platelet aggregability by Sienco aggregometer were measured. 24 hrs total estrogen in urine was also determined. In the control group, platelet counts were 85.1+ 4.9 % of the preoperated value one day after, 127.9+9.0 % one week after and 98.1+7.6 % one month after the operation. In the bilateral oophorectomy group, these were 82.4+5.2 % one day after, 124.0+4.7 % one week after and 96.1+4.8 % one month after. Both the groups showed the same change. Platelet aggregability by 3 μM ADP were 76.9+14.3 % one day after, 203.0+57.1 % one week after and 193.4+59.0 % one month after in the control, while 55.0+13.6 % one day after, 102.5+12.9 % one week after and 60.6+14.7 % one month after the operation in the total oophorectomy group. There was a statistically significant difference in the values obtained one month after the operation between the groups (p<0.05). Characteristic changes in platelet volumes were also observed. A significant correlation was observed between the platelet aggre-gabilities and the daily urinary estrogen excretion levels. The above results suggest that estrogen may enhance platelet aggregability in vivo.

The Effects Of Prostacyclin (PGI2) On Intravascular Platelet Aggregation

1981 ◽  
Author(s):  
G G Duncan ◽  
G Mallarkey ◽  
G M Smith
Keyword(s):  
Platelet Count ◽  
Guinea Pigs ◽  
Adenosine Diphosphate ◽  
Before And After ◽  
Dependent Inhibition ◽  
Induced Aggregation ◽  
Dose Dependent ◽  
Anaesthetised Rats

Intravascular aggregation can be measured by counting the number of circulating platelets before and after the injection of aggregation agents. The Technicon Autocounter was modified to count platelets continuously and connected via a double cannula in a carotid artery to an anaesthetised animal.Adenosine diphosphate (ADP) and collagen gave dose- dependent falls in the circulating platelet count when injected into rats, guinea pigs and rabbits. This enabled aggregation to be accurately quantitated in vivo.The infusion of PGI2 (0.25-1 ug/kg/min) in anaesthetised rats and rabbits produced a dose-dependent inhibition of the fall in platelet count produced by ADP and collagen. The formation of PGI2 can be inhibited in vitro by 15- hydroperoxyarachidonic acid (15HPAA). When 20 ug/kg/min of 15HPAA was infused into rats, aggregation produced by collagen was significantly increased suggesting that PGI2 is continuously formed by the rat vascular endothelium. This observation was confirmed by infusing 6-keto PGF1α antiserum. This antibody also prevented the inhibitory activity of PGI2 on collagen-induced aggregation. The study of continuous platelet counting in guinea pigs has been hampered by the occurrence of thrombocytopenia in certain animals. When 2 ug/kg/min of PGI2 was infused for 10 mins, a rise in the circulating platelet count to a steady plateau 4-5 × 105 platelets occurredThese experiments have shown that PGI2 will prevent aggregation by ADP and collagen and will reverse spontaneous thrombocytopenia and that PGI2 is continuously released from the vessels of anaesthetised rats.

A New Hexahedral Mesher for a Numerically Efficient Patient Specific Analysis of Arterial Blood Flow and Wall Shear Stress

2010 ◽  
Author(s):  
G. De Santis ◽  
P. Mortier ◽  
M. De Beule ◽  
P. Segers ◽  
P. Verdonck ◽  
...  
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Imaging Techniques ◽  
Arterial Blood Flow ◽  
Patient Specific ◽  
Arterial Tree ◽  
Arterial Blood ◽  
Current Measuring ◽  
Wall Shear

Atherosclerosis depends on systemic risk factors but manifests itself as geometrically focal plaques, which appear in regions of the arterial tree experiencing low and/or oscillating Wall Shear Stress (WSS) such as outer edges of vessels bifurcations and highly curved vessels. Because direct measurements of WSS (differential quantity) in vivo are difficult due to limited spatial resolution offered by current measuring technologies (ultrasound, phase contrast MRI), an indirect approach is often taken, integrating medical imaging techniques (biplane angiography, CT, MRI) with Computational Fluid Dynamics (CFD) for patient specific WSS profiling.

Human Platelet Aggregation and Release Reaction Induced by Platelet Activating Factor (PAF-Acether) – Effects of Acetylsalicylic Acid and External Ionized Calcium

1985 ◽  
Vol 53 (02) ◽  
pp. 221-224 ◽  
Author(s):  
Marco Cattaneo ◽  
Maria Teresa Canciani ◽  
Pier Mannuccio Mannucci
Keyword(s):  
Platelet Aggregation ◽  
Acetylsalicylic Acid ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Normal Subjects ◽  
Human Platelet Aggregation ◽  
Low Concentrations ◽  
Before And After ◽  
Platelet Secretion

SummaryThe effects of the cyclo-oxygenase inhibition on PAF-acether- induced human platelet aggregation and secretion are controversial. We studied the above parameters on citrated platelet-rich plasma of 12 normal subjects before and after the in vivo administration of acetylsalicylic acid (ASA). Individual sensitivities to PAF-acether were highly variable. ASA completely inhibited the platelet secretion induced by low concentrations of PAF-acether, but caused only partial inhibition when platelets were exposed to high concentrations of PAF-acether. The concentration of PAF-acether which overcame the cyclo-oxygenase inhibition varied substantially, depending on the individual sensitivity of the platelets to it. The addition of CaCl2 2 mM to the samples did not affect the extent of the platelet secretion, but increased irreversible aggregation in samples taken both before and after the ASA administration. These data suggest that low concentrations of PAF-acether stimulate the human platelet secretion by activating the cyclo-oxygenase pathway, whereas higher concentrations also trigger other mechanism(s) that suffice to induce human platelet secretion and full aggregation.

Slow postcapillary changes in blood pH in vivo: titration with acetazolamide

1978 ◽  
Vol 45 (4) ◽  
pp. 565-573 ◽  
Author(s):  
A. Bidani ◽  
E. D. Crandall
Keyword(s):  
Carbonic Anhydrase ◽  
Transport Processes ◽  
Arterial Blood ◽  
Blood Ph ◽  
Pulmonary Capillaries ◽  
Before And After ◽  
Time Courses ◽  
Electrode Chamber ◽  
Good Agreement

A stopped-flow pH electrode apparatus was used to investigate the mechanisms underlying slow changes in plasma pH (pHO) after blood leaves the pulmonary capillaries in carbonic anhydrase-inhibited animals. After acetazolamide was administered to an anesthetized dog or cat, arterial blood was withdrawn through the electrode apparatus into a syringe. Syringe movement was then suddenly stopped. Temperature and pHO of the blood in the electrode chamber were monitored both before and after blood withdrawal ceased. After stopping flow, pHO of the blood in the electrode chamber a) rose 0.02 after a dose of about 1 mg/kg acetazolamide; b) did not change after a dose of about 2 mg/kg acetazolamide; and c) fell 0.10 after a dose greater than about 5 mg/kg acetazolamide. With reasonable red cell and plasma carbonic anhydrase activities assumed for each dose level of acetazolamide, a computer model of the reaction and transport processes occurring in blood after gas exchange in the lung yielded predicted time courses of pHo that were in good agreement with the experimental results. The observed slow pHo changes are largely a result of disequilibrium of [H+] between red blood cells and plasma as blood leaves the pulmonary capillaries.

Coagulation-Related Effect of Bortezomib Treatment in Patients with Relapsed or Refractory Multiple Myeloma.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2733-2733
Author(s):  
Maurizio Zangari ◽  
Jose Guerrero ◽  
Federica Cavallo ◽  
Michael J. Burns ◽  
Keshava Prasad ◽  
...  
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Factor V Leiden ◽  
Coagulation Factors ◽  
Factor V ◽  
Post Dose ◽  
Platelet Surface ◽  
Induced Aggregation

Abstract Proteasomes inhibitors have been recently identified as potential agents, which can influence processes leading to thrombosis. We have previously reported a reduced incidence of deep vein thrombosis (DVT) in 69 patients enrolled in Total Therapy III and treated with (B), dexamethasone, thalidomide, cisplatin and doxorubicin with prophylactic anticoagulation. Patients with relapse MM, not previously exposed to B with normal baseline coagulation parameters (PT, PTT fibrinogen and platelet count) were eligible for the study. Except for the two PCR-based genotyping assays Factor V Leiden and Prothrombin Gene, which were assessed only at enrollment, in table one are listed coagulation factors serially assessed at baseline and within 1 hour after the first dose of B on day 1 and 4 of the first treatment cycle. Platelet Aggregation, with epinephrine, collagen, arachidonic acid, ADP and P- selectin by flow cytometry, were obtained at same time points. Results: Median values of coagulation factors pre and post B infusion are shown in table 1. Platelet count on platelet rich plasma (PRP) decreased after each B treatment (204.1±69.2 × 103 platelets/μL versus 160.8±50.3 × 103 platelets/μL). Platelet aggregation in PRP induced by 10 μM ADP was reduced by 20% and 29% in post-B on day one and four with p-values of 0.033 and 0.009 rispectively. Ristocetin induced platelet agglutination and epinephrine-induced aggregation were both negatively affected by B administration, p=0.0077 and p=0.034. Platelet aggregations elicited by collagen and arachidonic were not affected by B P-selectin expression on platelet surface was overall decrease with each agonist after B administration however no statistical differences were observed. In conclusion this pilot study has shown that even a short in vivo B exposure can significantly impaired platelet number and function and could explain clinical observations. Table 1 Test Day 1 Pre-dose Median Day 1 Post-dose Median Day 4 Pre-dose Median Day 4 Post-dose Median PT (sec) 13.4 13.85 13.55 14.4 PTT (sec) 17.35 26.2 26.95 25.5 Fibrinogen (mg/dL) 385 360 386 341.5 Protein C (70%–160%) 114 102 120 115 Protein S (65–140%) 89 85 92 92.5 Antithrombin II (190–127%) 98 97.5 100.5 102 APC Ration 2.345 2.33 2.3 2.22 T.T. (<20s) 18.2 17.9 17.7 19.45 D-Dimer (ug/mL) 0.56 0.5 0.5 0.59 Homocysteine (umol/L) 8.77 8.99 8.69 8.13

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