The progesterone produced by the corpus luteum stimulates the the glandular epithelium of the endometrium to secrete a glycogen-rich material.
The glands become wide, tortuous, and saccular, and the endometrium thickest because of the influence of progesterone and estrogen from the corpus luteum and because of increased fluid in the connective tissue.
As the spiral artery grows into the superficial compact layer of the endometrium, they become increasingly coiled. The venous network become complex and large lacunae (venous spaces) develop. Direct arterio-venous anastomoses are prominent features of this stage.
The Ischemic phase (if pregnancy does not occur)
Occur if oocyte is not fertilized.
Vascular changes occur, leading to ischemia due to the constriction of the spiral arteries due to decreased seretion of hormones by the corpus luteum and this gives the endometrium a pale appearance.
Towards the end of the ischemic phase, the spiral arteries become constricted for longer periods leading to venous stasis and patchy ischemic necrosis of in the superficial tissues.
This is followed by rupture of damaged vessel walls and blood seeps into the surrounding connective tissue.
Small pools of blood form and break through the endometrial surface, resulting in bleeding into the uterine lumen from the vagina.
As small pieces of the endometrium detach and pass into the uterine cavity, the torn ends of the arteries bleed into the uterine cavity resulting in a loss of about 20 80 ml of blood.
Eventually, over 3 to 5 days, the entire compact layer and most of the spongy layer of the endometrium are discarded in the menses.