Inside blood: flow, diffusion and selective binding

01 / Blood composition and transport

Cells and molecules share the circulation.

Blood carries cells, proteins, dissolved gases, nutrients and signaling molecules through a branching circulation. Its plasma is the fluid medium; red cells transport oxygen, white cells participate in immunity, and platelets contribute to hemostasis. These components interact with one another and with the vessel wall. Their behavior emerges from flow, diffusion and molecular binding, not from purposeful searching by individual molecules.^[1]

Circulation distributes hormones; local transport brings them near cells, and appropriate receptors enable responses. Broad delivery can therefore coexist with selective recognition.

02 / Convection and diffusion

Flow and diffusion act at different scales.

Convection carries substances with flowing blood between organs. Diffusion arises from thermal motion and redistributes substances down chemical-potential gradients over shorter distances, including between capillaries and tissue. Both processes operate simultaneously.

Cell size, deformability, vessel geometry and pressure affect microvascular flow. Red cells deform through small capillaries. Oxygen crosses membranes readily, while larger proteins encounter different barriers. The blood–brain barrier is more selective than many other capillary beds.

Some compounds circulate partly bound to carrier proteins. Binding can influence their free concentration, distribution and clearance. A measurement of total concentration may therefore answer a different question from a measurement of unbound concentration. Neither number, on its own, identifies how strongly every target tissue is responding.

03 / Molecular recognition

Affinity is a relationship between rates.

Molecular recognition depends on shape, charge, solvent interactions and flexibility. Proteins sample conformations, and binding partners can stabilize particular states. A rigid lock-and-key model omits these dynamics; many encounters do not produce sustained binding.

For a simple one-to-one binding model, the dissociation constant is Kd = koff / kon. The association rate constant describes formation of a complex; the dissociation rate constant describes its separation. Lower Kd means tighter equilibrium binding in that model. The reciprocal ratio, kon/koff, is an association constant, not Kd. Units and model assumptions matter.^[4]

Affinity also differs from efficacy. A ligand can bind strongly without activating a receptor. Some drugs favor an inactive state; others activate a signaling pathway. The Nobel Prize background on G protein-coupled receptors explains how binding at the cell surface can be translated into intracellular change without the signaling molecule entering the cell.^[2]

04 / Organized encounters

Cell adhesion and clotting involve the vessel wall.

At an injury, platelets adhere and activate while coagulation reactions help produce fibrin, stabilizing a plug. Blood clotting needs spatial control: a useful response at a damaged vessel can be dangerous in an intact circulation. Counting platelets is therefore different from measuring all aspects of their function or the coagulation system.^[1][3]

White cells can slow, adhere and cross activated endothelium through adhesion molecules and chemical cues. This is active migration across a vessel boundary into tissue, not simply swimming upstream or diffusing like a small molecule. Local signals and anatomy determine its direction.