Blood platelet-derived microparticles release and bubble formation after an open-sea air dive

2012 ◽  
Vol 37 (5) ◽  
pp. 888-892 ◽  
Author(s):  
Jean-Michel Pontier ◽  
Emmanuel Gempp ◽  
Mihaela Ignatescu
Keyword(s):  
Platelet Aggregation ◽  
Decompression Sickness ◽  
Blood Platelets ◽  
Water Immersion ◽  
Bubble Formation ◽  
Blood Platelet ◽  
Field Conditions ◽  
Control Group ◽  
Open Sea ◽  
Experimental Group

Bubble-induced platelet aggregation offers an index for evaluating decompression severity in humans and in a rat model of decompression sickness. Endothelial cells, blood platelets, or leukocytes shed microparticles (MP) upon activation and during cell apoptosis. The aim was to study blood platelet MP (PMP) release and bubble formation after a scuba-air dive in field conditions. Healthy, experienced divers were assigned to 1 experimental group (n = 10) with an open-sea air dive to 30 msw for 30 min and 1 control group (n = 5) during head-out water immersion for the same period. Bubble grades were monitored with a pulsed doppler according to Kissman Integrated Severity Score (KISS). Blood samples for platelet count (PC) and PMP (annexin V and CD41) were taken 1 h before and after exposure in both groups. The result showed a decrease in post-dive PC compared with pre-dive values in experimental group with no significant change in the control group. We observed a significant increase in PMP values after the dive while no change was revealed in the control group. There was a significant positive correlation between the PMP values after the dive and the KISS bubble score. The present study highlighted a relationship between the post-dive decrease in PC, platelet MP release, and bubble formation. Release of platelet MPs could reflect bubble-induced platelet aggregation and could play a key role in alteration of the coagulation. Further studies must investigate endothelial and leukocyte MP release in the same field conditions.

The Effect of Calcium and Magnesium on Rabbit Blood Platelet Aggregation in Vitro

1964 ◽  
Vol 12 (01) ◽  
pp. 179-200 ◽  
Author(s):  
Torstein Hovig
Keyword(s):  
Platelet Aggregation ◽  
Cation Exchange ◽  
Calcium Concentration ◽  
Blood Platelets ◽  
Blood Platelet ◽  
Rabbit Blood ◽  
Calcium And Magnesium ◽  
Induced Aggregation ◽  
Blood Platelet Aggregation

SummaryThe effect of calcium and magnesium on the aggregation of rabbit blood platelets in vitro was studied, with the following results:1. Platelet aggregation induced by ADP or collagen could be prevented by EGTA or EDTA. The aggregating effect was restored by recalcification. The effect was also restored by addition of magnesium in EDTA-PRP, but not in EGTA-PRP unless a surplus of calcium was present.2. Calcium remained in concentrations of the order of 0.15–0.25 mM after dialysis or cation exchange of plasma. Aggregation of washed platelets resuspended in such plasma could not be produced with ADP or collagen, unless the calcium concentration was increased or that magnesium was added.3. The adhesiveness of blood platelets to collagen was reduced in EGTA-PRP and EDTA-PRP. Release of ADP from platelets influenced by collagen could not be demonstrated either in EGTA-PRP (presence of magnesium) or in EDTA-PRP.4. It is concluded that calcium is a necessary factor both for the reaction leading to release of ADP and for the the aggregation produced by ADP.5. Thrombin induced aggregation of washed platelets suspended in tris-buffered saline in the presence of calcium. No effect of magnesium could be observed unless small quantities of calcium were present.

Different effect of l-NAME treatment on susceptibility to decompression sickness in male and female rats

2014 ◽  
Vol 39 (11) ◽  
pp. 1280-1285 ◽  
Author(s):  
Aleksandra Mazur ◽  
Peter Buzzacott ◽  
Kate Lambrechts ◽  
Qiong Wang ◽  
Marc Belhomme ◽  
...  
Keyword(s):  
Decompression Sickness ◽  
Tap Water ◽  
Bubble Formation ◽  
Female Rats ◽  
Control Group ◽  
No Production ◽  
Male And Female ◽  
Male And Female Rats ◽  
Expression Activity ◽  
No Bioavailability

Vascular bubble formation results from supersaturation during inadequate decompression contributes to endothelial injuries, which form the basis for the development of decompression sickness (DCS). Risk factors for DCS include increased age, weight–fat mass, decreased maximal oxygen uptake, chronic diseases, dehydration, and nitric oxide (NO) bioavailability. Production of NO is often affected by diving and its expression–activity varies between the genders. Little is known about the influence of sex on the risk of DCS. To study this relationship we used an animal model of Nω-nitro-l-arginine methyl ester (l-NAME) to induce decreased NO production. Male and female rats with diverse ages and weights were divided into 2 groups: treated with l-NAME (in tap water; 0.05 mg·mL–1 for 7 days) and a control group. To control the distribution of nitrogen among tissues, 2 different compression–decompression protocols were used. Results showed that l-NAME was significantly associated with increased DCS in female rats (p = 0.039) only. Weight was significant for both sexes (p = 0.01). The protocol with the highest estimated tissue pressures in the slower compartments was 2.6 times more likely to produce DCS than the protocol with the highest estimated tissue pressures in faster compartments. The outcome of this study had significantly different susceptibility to DCS after l-NAME treatment between the sexes, while l-NAME per se had no effect on the likelihood of DCS. The analysis also showed that for the appearance of DCS, the most significant factors were type of protocol and weight.

scholarly journals Ice Water Immersion as an Additional Method in Physiology Recovery in the Sport

2018 ◽  
Vol 1 (3) ◽  
pp. 15-22
Author(s):  
Jair Burboa ◽  
Felipe Godoy ◽  
María Soledad Riquelme ◽  
Eugenia Vivar ◽  
Maximiliano Barahona ◽  
...  
Keyword(s):  
Athletic Performance ◽  
Functional Performance ◽  
Water Immersion ◽  
Chronic Fatigue ◽  
Leg Pain ◽  
Control Group ◽  
Average Height ◽  
Active Recovery ◽  
Jump Test ◽  
Experimental Group

Objective: Soccer has a reduced overall recovery time. If these situations are not properly controlled they can cause the athlete chronic fatigue, an increase in delayed-onset muscle soreness (DOMS) and thus result in a decrease in athletic performance. There are several therapies that have attempted to improve athletic performance, decrease the percentage of injuries and results in soccer. Training and recovery instances are opportunities to find ways to address this issue. Understanding the physiology of recovery is essential to accelerate some processes, with the aim of shortening the times. Subjects: Cryotherapy could improve functional performance tests and decrease pain in soccer players. Our work design is an experimental prospective study. Method: Twenty subjects (10 experimental subjects and 10 control group subjects), between the ages of 17 and 23, who are members of a university men's soccer team, participated in the study. The following variables were controlled: power; the number of jumps, the average height of a jump in a 30-second continuous jump test, and DOMS perception through visual analog scale (VAS). Both groups shall be subjected to a more active recovery as well as elongation carried out by the coaching staff. In addition to this, the experimental group shall also be subjected to ice baths (42-47 °F) for three minutes. Results: We found significant statistical differences in the number of jumps and the power of the same in the control group, thus obtaining improvements. No significant differences were observed in either group for the average jump height and percentage yield variables. In the assessment of DOMS significant differences were observed, with a lower perception of DOMS seen in the experimental group. Conclusion: Ice baths provide favorable results in some aspects of the 30-second continuous jump test, decreasing the perception of leg pain and fatigue, and therefore they can be considered a valid alternative in the management of these athletes.

Impaired ristocetin–induced Platelet Aggregation in Whole Blood Assessed with a Multiplate© Analyser Suggests a New Mechanism of Antiplatelet Effect of Aspirin and Clopidogrel,

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 3362-3362 ◽  
Author(s):  
Annick Ankri ◽  
Anne Baranger ◽  
Isabelle Martin-Toutain ◽  
Yves Samson ◽  
Jean-Philippe Collet ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Antiplatelet Therapy ◽  
Whole Blood ◽  
Dual Antiplatelet Therapy ◽  
Blood Platelet ◽  
Normal Control Group ◽  
Control Group ◽  
Irreversible Inhibitor ◽  
Blood Samples ◽  
Before And After

Abstract Abstract 3362 The five channel computerized Whole Blood Aggregation instrument (Multiple Platelet Function Analyzer or Multiplate®), assesses platelet aggregation based on a modified whole blood impedance aggregation method. It permits platelet aggregation to be measured after adding commonly used agonists as arachidonic acid (ASPItest), ADP (ADPtest), collagen (COLtest), ristocetin (RISTOtest) and TRAP (TRAPtest), by detecting changes in electrical resistance in whole blood. Instrument handling is easy. Results are available within 9 minutes. Our objective was to evaluate the effect of aspirin (irreversible inhibitor of COX-1) and/or clopidogrel (irreversible inhibitor of the platelet P2Y12 receptor) on whole blood platelet aggregations induced by the 5 agonists using the Multiplate® in patients treated by aspirin and/or clopidogrel. Patients and controls. Two hundred and twenty two consecutive patients were recruited: 83 treated daily by 75 or 100 mg aspirin (group A); 42 treated daily by 75 mg clopidogrel (group C); 70 treated daily by 75 or 100 mg aspirin plus 75mg clopidogrel (group AC) and 27 who were daily on 100 mg aspirin before coronary intervention were tested 12 h after dual loading dose of aspirin between 75 et 500 mg and 75 to 900 mg clopidogrel according to cardiologists' recommendations: group loading aspirin-clopidogrel (LAC). Among group AC, 23 consecutive patients requiring intracranial stent placement of supra-aortic vessel were tested first at preoperative, without antiplatelet therapy, then 1 month after initiation of daily continuous dual antiplatelet therapy by 100 mg aspirin + 75mg clopidogrel. Ninety six volunteers without pathology or drugs influencing platelet functions constitute the normal control group (N). Blood samples. All patient and controls gave informed consent prior to blood sampling. Blood samples were collected by venipuncture or obtained from the arterial sheath directly into vacutainer Becton Dickinson tube containing 0.129M sodium citrate. Results. Patients under medication showing lower aggregation values than the arbitrary cutoff (fifth percentile of the aggregation in the normal control group was selected for each agonist) were classified as abnormal and having biological sensitivity to the agonist tested. Aggregation values above the cutoff with ASPItest or ADPtest for patients on antiplatelet agents were considered as a persistent platelet aggregation and as a biological resistance. According to the literature, resistance to aspirin was found in 8.6% of patients under aspirin alone or in combination and in 25.1% of patients under clopidogrel alone or in combination. Our main result shows an inhibition in platelet aggregation using ristocetin as agonist for 73.9% of patients taking aspirin alone, for 27.8% on clopidogrel and in 94% of patients receiving combination of the 2 drugs. This inhibition appears after aspirin + clopidogrel intake as we could observe it among patients candidates for intracranial stent placement tested before and after one month of treatment by dual antiplatelet therapy. This effect is not related to von Willebrand Factor (vWF) deficiency since the measurement of ristocetin cofactor activity, and vWF antigen carried out among 14 patients exhibiting an inhibition in whole blood platelet aggregation using RISTOtest were normal and unchanged before and after antiplatelet treatment. VWF is essential platelet-to-platelet interactions which is promoted by the binding of VWF with platelet-receptor glycoprotein IbIX (GPIbIX). Our results suggest: 1) aspirin inhibits the interaction of vWF to GP IbIX. This inhibition appears increased by the association of clopidogrel to aspirin. 2) a new mechanism of inhibition of the platelet function GPIbIX-vWF dependant conjointly to inhibition of cyclooxygenase by aspirin and P2Y12 receptor by clopidogrel.Table I:Biological sensibility according to the five tests (%) in the 4 groups testedGroup (n)ASPItestADPtestCOLtestRISTOtestTRAPtestA (83)84.312.038.373.98.4C (42)38.176.219.227.816.7AC (70)90.074.348.288.222.9LAC (27)100.074.163.0100.029.6 Disclosures: No relevant conflicts of interest to declare.

Therapy with acetylsalicylic acid does not interfere with oral surgery

Open Medicine ◽  
2013 ◽  
Vol 8 (4) ◽  
pp. 392-397 ◽  
Author(s):  
Damian Dudek ◽  
Krzysztof Helewski ◽  
Grzegorz Wyrobiec ◽  
Marzena Harabin-Słowińska ◽  
Grażyna Kowalczyk-Ziomek ◽  
...  
Keyword(s):  
Heart Disease ◽  
Platelet Aggregation ◽  
Acetylsalicylic Acid ◽  
Oral Surgery ◽  
Thrombus Formation ◽  
Heart Diseases ◽  
Blood Platelets ◽  
Control Group ◽  
Drug Discontinuation ◽  
Significant Group

AbstractThe acetylsalicylic acid (ASA) treatment is widespread therapeutic strategy in cardiology clinics. On the other hand, patients with heart diseases represent a significant group of cases in dental clinics. Accordingly, we studied the local hemostatic thrombus formation after dental tooth extractions (n=47) and other oral surgery treatment (n=13) in 60 patients with heart disease being on ASA therapy without drug discontinuation. In the control group free of ASA therapy it was: (n=24) and (n=6), respectively. In all studied patients, the aggregative activity of blood platelets by PFA-100 analyzer was assessed. It was found that 61.7% patients treated with ASA presented inhibition of platelets aggregation. Unexpectedly, in 35% of such patients, platelet aggregation function remained unchanged. In the control group, normal platelet aggregation was found in all subjects. It has been shown that ASA therapy has neutral effects on both thrombus formation and pain complications in patients with heart disease underwent tooth extraction and other oral surgery. Thus discontinuation of ASA therapy before surgery seems to be weakly validated.

scholarly journals CAUSES OF THE DEVELOPMENT OF CORONARY SYNDROME X IN WOMEN

2020 ◽  
Vol 20 (3) ◽  
pp. 148-152
Author(s):  
I.V. Tsiganenko ◽  
L.K. Ovcharenko
Keyword(s):  
Endothelial Cells ◽  
Platelet Aggregation ◽  
Vascular Endothelium ◽  
Density Lipoprotein ◽  
Biologically Active ◽  
Syndrome X ◽  
Control Group ◽  
Coronary Syndrome ◽  
Experimental Group ◽  
Active Substances

The work considers the causes of the coronary X syndrome development in women by assessing the experimental group and the control group with typical angina pectoris with angiographically altered vessels. Each group included 30 patients. When studingy medical records of the patients in the study group, we found out that in the reproductive period all of them had hyperestrogenemia, confirmed by the laboratory data, with the corresponding consequences in the form of various gynecological diseases, while the patients of the control group had unburdened gynaecological history. In terms of the lipid spectrum, the results turned out to be opposite. In the experimental group, the rates were within the normal range, and the control level of LDL-C significantly exceeded the required values. Despite the fact that estrogens increase the concentration of high density lipoprotein (HDL) in the blood and lower the content of low density lipoprotein (LDL) that are atherogenic, their surplus has a less negative effect than their lack, as the risk of developing atherosclerosis increases with decreasing concentration, and with an increase there is a risk of developing endothelial dysfunction, which provokes the development of coronary syndrome X. These date confirm the development of endothelial dysfunction in the patients of the experimental group with hyperestrogenemia in the history resulted from the impairment of the process of proliferation of endothelial cells with subsequent imbalance of secretion of biologically active substances. Among them, there is nitric oxide, which causes the relaxation of smooth myocytes, thus resulting in vasodilatation, and endothelins, providing the opposite, vasodilating effect. Prostacyclines and thrombomodulins secreted by the vascular endothelium in physiological conditions, counteract platelet aggregation. In the case of damage to the vascular wall, the production of prostacyclin and thrombomodulin is suppressed, but the release of thromboplastin, platelet activation factor and von Willerband factor activates that promote platelet aggregation and blood clotting. Under the participation of other physiologically active substances, selectins, endothelial cells promote adhesion to their surface and further penetration into the site of inflammation of neutrophils, blood acidophils. Selectin is accumulated in the cytoplasm of the endothelial cells in the form of specific electron-cellular inclusions, the so-called bodies of Weibel-Palade. Normally, vascular endothelium is impervious to blood components. However, being affected by a number of factors, and in particular histamine, endothelial cells lose contact with each other and decrease in number. This leads to the release of water and plasma proteins into the intercellular medium causing oedema. Due to the ability of the inner layer of vessels to produce a large number of biologically active substances, such changes can hardly be corrected by therapy.

The Effect Of A Proteinase Inhibitor On Platelet Function In Stored Blood

1981 ◽  
Author(s):  
S Haas ◽  
P Wendt ◽  
G Blümel
Keyword(s):  
Platelet Aggregation ◽  
Proteinase Inhibitor ◽  
Blood Platelets ◽  
Bleeding Risk ◽  
Control Group ◽  
High Dose ◽  
Aggregate Formation ◽  
Blood Samples ◽  
Stabilizing Effect ◽  
Stored Blood

Blood platelets are markedly traumatized by the withdrawal of blood from the donor. Hereby the function of thrombocytes is activated and this platelet stimulation is closely related with the early formation of microaggregates in stored blood. Therefore it is clinically desired to stabilize the platelets but without inhibiting their function irreversibly and causing hemorrhage. Concerning this question an experimental study was carried out.Blood was drawn from 10 volunteers under blood bank conditions and was stored in presence of 200 KIU aprotinin per ml ACD-blood resp.the same volume of saline at a temperature of +4°C. Immediately after the withdrawal of blood and 1,2,3 and 7 days later blood samples were taken and the following parameters were studied: platelet aggregation induced by ADP, aggregate ratio, PF 4, beta-thromboglobulin and tx B2 in plasma and serum.In the aprotinin blood the aggregability was slightly diminished and was longer present than in the control group. In addition, the aggregate formation was significantly decreased. The release reaction of platelets was not effected by aprotinin;the increase of PF 4 and beta-thromboglobulin was similar to that of the control group. Also the thromboxane formation was not effected. Thus the protective effect of aprotinin is independent from the prostaglandin metabolismThis study shows that a high dose of aprotinin has a stabilizing effect on platelets in stored blood and that the thrombocyte function is not irreversibly inhibited by this substance. Therefore, aprotinin can be regarded to be effective in the prophylaxis of disseminated platelet aggregation without causing a bleeding risk.

BLOOD PLATELET FUNCTION OF HYPERLIPIDEMIC PATIENTS TREATED WITH BEZAFIBRATE

1987 ◽  
Author(s):  
A Borowska
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Blood Platelet ◽  
Clofibric Acid ◽  
New Drugs ◽  
Control Group ◽  
Lipid Levels ◽  
Before And After ◽  
600Mg Daily ◽  
Layer Chromatography

Platelets from patients with hyperlipoproteinemia (HLP) are more sensitive to some aggregating agents than platelets from normal persons.On the other hand, it is known that from 15% to 20% of patients with coronary heart disease have primary or secondary HLP.The progress of the knowledge in this field has been expressed in production of the new drugs diminishing HLP.Be-zafibrate is a new derivative of clofibric acid,which has been used in the treatment of HLP.The purpose of our study was and assessment of the effect of bezafi-brate on platelet aggregation and thromboxane (TXB2) generation.The experiments were carried out in 18 patients (7 women and 11 men),aged 32-60 (mean 46 years) with type Ila HLP.The control group of consisted of 10 healthy volunteers.For 6 weeks the patients with HLP were given bezafibrate (Bezalip-Boehringer Mannheim) 600mg daily in divided doses and were taking the same diet as before the treatment.Blood platelet aggregation and 14C arachidonic acid (AA) conversion to thromboxane in washed platelets (using thin-layer-chromatography) were determined before and after bezafibrate administration. The obtained results are presented in the table (mean±S.E.).It is concluded that the main arteriosclerosis-protecting bezafibrate action lies not only in decreasing of lipid levels in serum, but also in normalization of platelet function.

scholarly journals Functional properties of hemostasis in piglets after short-term overheating against the background of corrective action

2020 ◽  
Vol 17 ◽  
pp. 00169
Author(s):  
Vladimir V. Zaitsev ◽  
Marina V. Mekhanikova ◽  
Svetlana V. Shestakova ◽  
Tatyana P. Ryzhakina
Keyword(s):  
Platelet Aggregation ◽  
Control Group ◽  
Platelet Activity ◽  
Large White ◽  
White Breed ◽  
Negative Effect ◽  
Group A ◽  
Group 2 ◽  
Experimental Group ◽  
Group 1

Catosal is considered to be a highly effective bio-stimulator. It showed his properties in animals, realizing the stimulation of their tissues and organs. The purpose of this research is to determine the effect of Catosal on hemostatic parameters in piglets that experienced overheating. 58 piglets at the age of 2.5 months, which belonged to a large white breed, were taken into work. All animals as a result of an accidental emergency shutdown of the air conditioning system in the pigsty suffered overheating for 3 hours. These animals were randomly divided into two comparable groups. One was named experimental; the other was called control 1. Pigs of the experimental group (21 heads) received intramuscular injections of 2.5 ml of Catosal daily for 5 consecutive days, from the next day after an overheating episode. The control group 1 consisted of piglets with a total number of 21. After an overheating episode, they were under the usual conditions of a pigsty and did not receive any effects. In experimental piglets and piglets of the control group 1, all indicators were recorded in the outcome and after 30 days. Control group 2 consisted of 32 completely healthy piglets that were kept under standard conditions of a pigsty for their entire lives. They were examined once. Catosal injections in the observed piglets after overheating led to a decrease in spontaneous and stimulated platelet aggregation to normal levels. Against the background of the use of Catosal in the piglets that made up the experimental group, a weakening of hemocoagulation was found, which improved blood circulation in their tissues. Piglets of control group 1 showed an increase in platelet aggregation and blood coagulation. This had a very negative effect on hemorheology in them and weakened their metabolism. We can assume that in piglets after overheating, in the absence of optimizing effects, hemostasis is activated. This adversely affects the course of microcirculation and inhibits growth. Injections in piglets after overheating of the Catosal lead to a weakening of hemocoagulation and platelet activity to optimum values. This normalizes the course of microcirculation in the internal organs of animals.

IN VIVO CHANGES IN SYSTEMIC PCO2 AND PO2 INFLUENCE THE THROMBOEMBOLIC REACTION FOLLOWING WALL PUNCTURE IN VENULES BUT NOT IN ARTERIOLES

1987 ◽  
Author(s):  
Mirjam G A oude Egbrink ◽  
Geert Jan Tangelder ◽  
Dick W Slaaf ◽  
Robert S Reneman
Keyword(s):  
Thrombus Formation ◽  
Fluid Dynamic ◽  
Blood Platelets ◽  
Control Group ◽  
Blood Gas ◽  
Systemic Blood ◽  
Normal Ranges ◽  
Experimental Group

Changes in pH and PCO2 influence the aggregation of blood platelets in response to various agents in vitro. In the present study intravital video-microscopy was used to investigate whether changes in systemic blood gas values influence the thromboembolic reaction in vivo as induced by vessel wall injury.The microtrauma was induced by puncturing the walls of microvessels in the rabbit mesentery (diameter range: 20-40 μm) with glass micropipets (tip diameters: 6-8 μm). The thromboembolic reactions were compared in two groups of anesthetized rabbits. The control group was ventilated to keep the blood gas values within normal ranges (means: pH=7.40, pCO2=32.9 mmHg, pO2=104.7 mmHg). The experimental group breathed spontaneously (mean blood gas values: pH=7.34, pCO2=50.5 mmHg, pO2=48.1 mmHg). The pCO2 and pO2 values were significantly different between both groups.In arterioles and venules of both groups bleeding and thrombus formation started immediately following wall puncture. Bleeding times were short (medians between 1.0 and 2.6 s). Parts of the thrombi started to embolize between 11.4 and 18.2 s following wall puncture (medians). In the control group embolization continued for 101 s in the arterioles and 17 s in the venules; during these periods 6 and 1 emboli were produced, respectively (all median values). In the experimental group the duration of embolization in the arterioles was 143 s in which period 7.5 emboli were produced, values not significantly different from control. In the venules of the experimental group embolization and hence platelet reaction went on uninhibited during the whole observation period of 600 s and 30 emboli were produced. Fluid dynamic factors cannot explain the differences in thromboembolic reaction between the control and experimental venules; vessel diameters and red blood cell velocities were not significantly different between both groups. Therefore, it is likely that the change in thromboembolic reaction in the venules results from the changes in systemic PCO2 and/or pO2. The different reactions in arterioles and venules in response to the altered systemic blood gas values might arise from different reactions in the vessel walls.

Sign in / Sign up

Export Citation Format

Share Document