{'fraction_non_alphanumeric': 0.023928215353938187, 'fraction_numerical': 0.0, 'mean_word_length': 5.6490066225165565, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Prostaglandins and the non-pregnant uterus. The pathophysiology of primary dysmenorrhea.

The biochemical background of primary dysmenorrhea is characterized by high uterine prostaglandin levels, high levels of blood arginine vasopressin and of estradiol in the late cycle. In dysmenorrheic patients the progesterone level is slightly higher when bleeding starts, than in eumenorrheic patients, but is normal during the late cycle. Biochemical actions pass through free 'activator' calcium, and this, together with possible micro-anatomic changes (like increased frequency of gap junctions), explains the smooth-muscle dysfunction. The uterine activity is characterized by high conduction velocity (as indicated by the high rate of rise in active pressure) and by high resting pressure. The pathophysiology of primary dysmenorrhea includes diminished uterine blood flow and anoxic pain, which result from the constriction of the uterine arteries and/or from the contracture on the uterine muscle itself.