In the periovulatory phase, the LH surge triggers ovulation. Which of the following mediates the final rupture of the follicle wall?
- A LH surge induces prostaglandin synthesis (PGE2 and PGF2α) and matrix metalloproteinases (MMPs) in the follicle wall, causing dissolution of the extracellular matrix and smooth muscle contraction for follicular rupture ✓
- B LH surge causes rapid follicular fluid pressure increase due to osmotic expansion, mechanically rupturing the follicle
- C LH directly activates plasminogen activator in granulosa cells, producing plasmin that dissolves the zona pellucida, releasing the oocyte
- D Oestrogen surge immediately prior to the LH peak causes apical follicle wall necrosis, allowing passive oocyte release
Explanation
The LH surge triggers a complex inflammatory-like cascade in the follicle wall. LH via cAMP activates granulosa cells and thecal cells to produce arachidonic acid metabolites, particularly prostaglandin E2 (PGE2) and PGF2α, and to upregulate proteolytic enzymes including matrix metalloproteinases (MMP-1, MMP-2, ADAMTS) that degrade collagen and ECG in the follicle wall apex. LH also induces the expression of VEGF (causing hyperaemia) and activates the protease cascade (plasminogen activator → plasmin). Smooth muscle cells in the theca contract under prostaglandin and oxytocin stimulation. Together, these cause controlled digestion and rupture of the follicle apex, releasing the cumulus-oocyte complex. Indomethacin (COX inhibitor) blocks prostaglandin synthesis and prevents ovulation. Option B is incorrect; osmotic pressure is not the mechanism. Options C and D are partial or incorrect descriptions.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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