Within minutes of intradermal histamine release, fluid escapes into the interstitium through postcapillary venules. Which mechanism accounts for this early increase in vascular permeability?
- A Contraction of endothelial cells opening intercellular gaps ✓
- B Leukocyte-mediated endothelial injury
- C Direct necrosis of the entire vessel wall
- D Increased transcytosis through the vesiculovacuolar organelle
Explanation
Histamine, bradykinin, and leukotrienes bind receptors on venular endothelium and trigger actin-myosin contraction, producing reversible gaps between cells. This is the immediate transient response, peaking within minutes and lasting 15 to 30 minutes, and it affects venules 20 to 60 micrometers in diameter, not capillaries or arterioles. Direct endothelial injury produces a delayed prolonged leak beginning hours later, and leukocyte injury occurs only after emigration, both too slow for this scenario.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.