Platelet aggregation - this is a normal physiological process that allows you to quickly stop the internal or external bleeding, as well as to stimulate the repair of damaged tissues. Sticking (adhesion) specific platelets, which are responsible for blood clotting, is not the only step in hemostasis. However, an increase or decrease in the activity of the process by the action of drugs and pathological factors (diseases) can lead to a critical loss of blood and severe complications.
What is platelet aggregation, and what role the body plays in this process
Aggregation - this gradual accumulation of a plurality of similar cells (platelets) around a small center in the point of injury. Enlargement controlled natural clot inducers - substances which are released upon tissue damage. Depending on the size of a certain amount of damage is activated platelets and partially Activated platelets are separated from the conglomerate created (unit) and returned to the bloodstream. This reverse process of accumulation is called disaggregation.
Step platelet aggregation is the third in the process of stopping bleeding. First, upon receipt of the fault signal, CNS provokes ruptured vessel spasm and platelet adhesion then occurs in the blood to close the hole in the vessel.
After adhesion formation begins thrombocyte aggregates, which completes the irreversible aggregation - forming a loose tube. The final step is to seal the platelet plug under the action of thromboplastin and fibrin.
Preparation for analysis
Blood tests to determine the clot accumulation rate is carried out on an empty stomach. Since the last meal prior to blood sampling should be at least 6-8 hours.
To ensure the accuracy of the result of the patient is necessary to observe the following guidelines:
- a day before the visit of the laboratory center to abandon sports loads and consumption of alcoholic drinks, possible to eliminate stress;
- 1-2 days prior to study the use of alcohol;
- does not smoke at least 3-6 hours prior to analysis;
- deleted reception antiplatelet agents and other agents affecting blood clotting (including NSAIDs diclofenac, aspirin, indomethacin, paracetamol, etc.).
Independently cancel ongoing drug therapy for blood donation can not. In some cases (e.g., at high risk of ischemic stroke and heart attack) cancellation can lead to serious complications. At constant treatment antisvertyvayuschey means to warn doctors and laboratory on the composition of therapy.
Terms of delivery of the analysis are not a recommendation, but mandatory because nicotine, NSAIDs and adrenaline, which released during stress and physical stress, a direct impact on the formation of thrombocyte conglomerates.
research methods
For the diagnosis of pathological states is necessary to know not only the effect of platelet aggregation, and what it is, but also the normal characteristics of this process under different conditions.
To determine the ability of the aggregation of blood cells using special devices - aggregometry. They allow you to record and automatically analyze all the events that happen to blood cells. The data is displayed in the email (numeric) and graphical form.
Under laboratory conditions tested spontaneous and induced platelet aggregation.
In the human body substance-inducers (instigators clusters of cells) protrude adrenaline (epinephrine), collagen, adenosine triphosphate, von Willebrand factor and other compounds. As laboratory reagents used substances which are synthetic analogs of inducers or provoke the production of natural aggregation factors.
In order to accurately differentiate the pathology and reduce the influence of extraneous factors on the accuracy of the analysis, the study is carried out with 3-5 inductors.
With ristotsetin
Ristocetin (ristomycin) - is an antibacterial drug which is mainly used as inducer reagent in assays for platelet aggregation.
The mechanism of action of the method based on the ability ristomycin affect the interaction of vWF with one of glycoproteins, provide attachment blood cells to the site of injury. In the absence of this factor inactive glycoprotein is rapidly degraded in the bloodstream.
In some genetic pathologies observed normal platelet response to the impact of other inducers (epinephrine, ADP, etc.). However, the results of studies using ristocetin observed significant violations.
When deviations are detected for more differential diagnosis in biomaterial added normal plasma. Normalization process or repeated pathological result indicates the root cause of the deviation.
collagen
Collagen is a natural inducer of aggregation. Contact this connective tissue protein means blood, that some portion of the vessel were damaged.
The process of formation of collagen with the assistance unit is sufficiently long latency period. During the latent phase of activation of blood occurs enzyme (phospholipase). Depending on the concentration of inducer laboratory preparation for the duration of the reaction may be up to several minutes.
After completion of the latent period in blood cells formed secondary reagents (including thromboxane A2) which dramatically increase the intensity of the platelet interaction.
The accuracy of the test result depends on the correct interpretation of the data and the type of reagent. The most common laboratory collagen concentration is 50 ng / l. In another concentration inducer substance duration of the lag phase varies accordingly.
With adrenaline
Adrenal hormone epinephrine receptors interact with adrenaline and causes significant inhibition of the enzyme adenylate cyclase. This increases the rate of formation of thromboxane, provoking the active aggregation of blood cells.
Thromboxane aggregation mechanism may account for only a second wave process. Start the reaction by some researchers to explain the direct influence of epinephrine on the permeability of cell membranes and transport of calcium ions.
Adrenaline-induced blood platelet aggregation study eliminates the most common disease of the coagulation system.
C arachidonic acid
Arachidonic acid, which belongs to the group of polyunsaturated fatty acids (PZHNK) omega-6, is a natural platelet stimulator forming conglomerates.
The mechanism of action of this PUFA is complex: it influences the synthesis of inflammatory factors (prostaglandins), thromboxane, phospholipases C and A2. Activation of phospholipase first lead to the mobilization of calcium ions within the cells, activation of more platelets and release of secondary mediators process. Activation of phospholipase A2 releases its own (endogenous) arachidonic acid, which further accelerates aggregation.
Due to the complex action and release of endogenous PZHNK aggregate formation occurs sufficiently rapidly and is not split into two waves.
Analysis PZHNK inducer allows to differentiate pathology aggregation and result of prolonged use of antiplatelet agents (NSAIDs, certain antibiotics, diuretics and others.). When receiving antiplatelet agents with arachidonic acid sample is negative.
With adenosine triphosphate
Character adenosine exposure depends on its concentration. When a small dosage ADP aggregation takes place in two waves due to the fact that unconcentrated reagent catalyzes its own release inductors process. Initial, small wave formation is provoked by external units (exogenous) ADP.
Large doses of adenosine triphosphate (more than 6.10 mol) cause a strong reaction, so the process flow into two waves into one.
When analyzing the results of the research lab technician draws the attention of both the numerical data (process speed), and the kind of agregatogrammy. The deviation from the normal graphic form (e.g., reversible aggregation in response to ADP administration of large doses) indicates the nature of the pathology: Sensitivity violation clotting blood cells, platelets, and slow release et al.
No less important than the induced formation of the conglomerate, it is the spontaneous aggregation of platelets (CAT). This process is studied without inducers substances. SAT intensity is determined based on morphological characteristics and visual methods.
Increased spontaneous aggregation is a dangerous phenomenon, because does not depend on tissue damage occurs in the microvasculature, which increases the risk of thrombosis.
normal levels
The normal degree of aggregation depends on the concentration and type of inducer agent:
- reaction with collagen (concentration reagent - 5, and 10 ug / mL) rate is 75% and 93.1%, respectively;
- with epinephrine (150 and 300 .mu.mol) - 46% and 92.5%;
- ADP (up to 5 micromole and 5-10 micromole) - less than 66% and 66,1-77,7%.
In assays ristomycin arachidonic acid and the result is determined positive or negative reaction.
The normal concentration of platelets in blood analysis in this case is 180-400 U / NL according to the sex, age and condition of the patient.
Gipoagregatsiya
Gipoagregatsiya platelets - this pathology, in which the rate of formation of aggregate or activated blood cells is reduced.
Causes
Gipoagregatsii may accompany such diseases:
- receiving dosage aggregation inhibitors (NSAIDs, muscle relaxants, beta-lactam antibiotics, sedatives, diuretics, anticoagulants large doses et al.);
- alcohol abuse;
- administration of solutions of dextrans (e.g. reopoligljukin);
- hematopoietic disorders, including due to malnutrition;
- infectious and inflammatory diseases;
- hereditary and genetic diseases (von Willebrand's disease, Wiskott-Aldrich);
- uremia et al.
This may precede severe injury, which result in massive cell aggregation first, followed by shock (DIC).
Treatment
To increase the aggregation rate applied glucocorticosteroids (prednisone, hydrocortisone), amino acids, ATP, iron supplementation and other micronutrients Dicynonum, Emosint.
Effects
Gipoagregatsiya can cause severe blood loss even at minor external damage and massive internal bleeding.
hyperaggregation
Hyperaggregation - a condition in which the rate of formation of conglomerates of blood abnormally increased.
why is there
hyperaggregation reasons could be:
- Gastrointestinal and urinary tract diseases;
- leukemias;
- atherosclerosis and hypertension;
- endocrine diseases (including diabetes mellitus);
- medications that increase blood clotting;
- Hodgkin's disease;
- sepsis et al.
Therapy
To treat this condition and prevent its complications applied antiplatelet agents (including NSAIDs), blood transfusion substitute, anticoagulants and drugs that reduce vascular tone.
The dangerous
Hyperaggregation blood cells provoke the formation of thrombi and acute circulatory disorders of internal organs (brain, heart, kidneys, etc.). Increase the intensity of aggregation during pregnancy can cause miscarriage.
