Morphology and Ultrastructure of the Granulomere Zone
When examining a blood smear stained with Romanowsky stain, two distinct structural zones are visible in platelets: the stained granulomere (chromomere) in the center and the pale hyalomere at the periphery.
The ultrastructure of the granulomere is represented by general organelles (elements of the endoplasmic reticulum, mitochondria, ribosomes, peroxisomes), glycogen particles, lysosomes (γ-granules), and two main types of specific granules:
- α-granules (alpha-granules): contain high-molecular-weight proteins. These include coagulation factors (fibrinogen, factor XIII), growth factors stimulating cell proliferation during vascular wall regeneration, and hydrolytic enzymes.
- δ-granules (delta-granules / dense granules): store low-molecular-weight compounds. They contain Ca²⁺ ions as well as biogenic amines—histamine, epinephrine, and serotonin (taken up by the platelet from the plasma).
Organization of the Hyalomere and Surface Apparatus
The peripheral zone of the platelet—the hyalomere—ensures maintenance of shape, movement, and secretion. It contains:
- Dense tubular system: derivatives of smooth endoplasmic reticulum serving as a store for Ca²⁺ ions. Here, with the participation of the enzyme cyclooxygenase, prostaglandins and thromboxanes are synthesized from arachidonic acid as 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: invaginations of the plasmalemma designed for the release of granule contents into the extracellular environment.
- Plasmalemma and Glycocalyx: the platelet membrane possesses a robust glycocalyx, carries ABO blood group antigens and specific receptors. The negative charge of the membrane, due to phosphate groups of phospholipids and phosphoproteins, is critical for binding coagulation factors.
Mechanism of Platelet Participation in Hemostasis
The platelet response to vascular wall injury unfolds sequentially:
- 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.
- 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.
- 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 carboxyl groups of plasma clotting factors. Factors II and VII are present on the membrane initially, while factors X and V attach after activation. Fibrinogen is converted into fibrin, whose strands entrap the clot and trap erythrocytes.
- Clot retraction: factor XIII (fibrin-stabilizing factor, transglutaminase) is released from α-granules, catalyzing cross-links between fibrin molecules to transform the soft clot into a sturdy thrombus.