Platelets

Morphology and ultrastructure of the granulomere zone

When examining a blood smear stained with Romanowsky's method, two structural zones are clearly distinguished in platelets: the stained granulomere (chromomere) in the center and the light hyalomere at the periphery.

The ultrastructure of the granulomere is represented by general-purpose organelles (elements of the endoplasmic reticulum, mitochondria, ribosomes, peroxisomes), glycogen clumps, lysosomes (γ-granules), and specific granules of two main types:

• α-granules (alpha granules): contain high-molecular-weight protein substances. Their composition includes coagulation factors (fibrinogen, factor XIII), growth factors that stimulate cell proliferation during vascular wall regeneration, and hydrolytic enzymes.
• δ-granules (delta granules): accumulate low-molecular-weight compounds. They contain Ca²⁺ ions, as well as biogenic amines — histamine, adrenaline, and serotonin (uptaken by the platelet from plasma).

Organization of the hyalomere and surface apparatus

The peripheral zone of the platelet — the hyalomere — ensures maintenance of shape, movement, and secretion. It localizes:

• Dense tubular system: derivatives of the smooth endoplasmic reticulum, serving as a depot for Ca²⁺ ions. Here, with the participation of the enzyme cyclooxygenase from arachidonic acid, prostaglandins and thromboxanes are synthesized — regulators of aggregation and vascular tone.
• Cytoskeleton: a bundle of 4–10 microtubules forms a marginal band to maintain the discoid shape at rest. Actin microfilaments are distributed throughout the volume and, together with microtubules, ensure the formation of processes (pseudopodia) upon activation.
• Open canalicular system: plasmalemma invaginations intended for excreting granule contents into the external environment.

The platelet plasmalemma possesses a powerful glycocalyx, carries ABO system antigens and specific receptors. The negative charge of the membrane, due to phosphate groups of phospholipids and phosphoproteins, is critically important for binding coagulation factors.

Mechanism of platelet involvement in hemostasis

The platelet response to vascular wall injury unfolds sequentially:

1. Formation of the primary ("white") thrombus: under the influence of biologically active substances (including ADP), platelets adhere to the damaged wall (adhesion) and stick to each other (aggregation). Upon activation, they change shape, forming long, thin pseudopodia.
2. Vascular spasm: release of serotonin from δ-granules and thromboxanes from the dense tubular system causes narrowing of the vessel lumen to reduce blood loss.
3. Formation of the "red" thrombus: a cascade of enzymatic reactions occurs directly on the plasmalemma. Calcium ions (Ca²⁺) form chelate ("claw-like") complexes, simultaneously binding to the phosphate groups of the membrane and the carboxyl groups of plasma coagulation factors. Factors II and VII are initially present on the membrane, while factors X and V join after activation. Fibrinogen is converted into fibrin, the strands of which entangle the clot and trap erythrocytes.
4. Thrombus retraction: factor XIII (fibrin-stabilizing factor, transglutaminase) is released from α-granules, which catalyzes cross-links between fibrin molecules, transforming the soft clot into a dense thrombus.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Ultrastructure and functions of the marginal microtubule band at rest and during activation
• Mechanism of thromboxane synthesis from arachidonic acid in the dense tubular system
• Structure of the open canalicular system and the process of granule content exocytosis
• Dynamics of the binding of coagulation factors X and V to the platelet surface apparatus
• Role of α-granule growth factors in cell proliferation and vascular wall regeneration

Other topics in the "Blood" section

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