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大量详细的证据支持前列腺素(PG)在痛经的病理生理中起作用。PGF_(2α)可能通过增加子宫收缩性引起痛经。把PGF_(2α)灌注到子宫内引起痛经样疼痛,甚至导致月经样出血。支持这种机制的进一步证据来自以下发现:PG合成的抑制药是治疗痛经的有效药物。这些药物也减少子宫的收缩性。但至今还无人试图说明原发性痛经患者月经血中PG的浓度与子宫收缩类型的关系,及与对照组的比较。本文的目的是完成这些工作。受试者为24名未产妇女。无妇科疾病,未用口服避孕药或节育环。骨盆检查正常。痛经组的13名妇女从十几岁即因严重痛经不能工作而就医。对温和的镇痛药如Paracetamol或阿斯匹林无反应。11名对照者最多有轻度不适,很少需用镇痛药。两组一般特点无明显不同。每日将月经液收集到一个避孕用隔膜中,三小时后取出隔膜并测定容积。用以前描述的方法提取月经液中的PGF_(2α)和PGE_2。
A large body of detailed evidence supports the role of prostaglandins (PGs) in the pathophysiology of dysmenorrhea. PGF_ (2α) may cause dysmenorrhea by increasing uterine contractility. PGF_ (2α) perfusion into the uterus causes dysmenorrhea pain, and even lead to menstrual bleeding. Further evidence to support this mechanism comes from the discovery that inhibitors of PG synthesis are potent drugs for the treatment of dysmenorrhea. These drugs also reduce uterine contractility. However, no attempt has been made so far to elucidate the relationship between the concentration of PG in menstrual blood and the type of uterine contractions in patients with primary dysmenorrhea, as compared with the control group. The purpose of this article is to accomplish these tasks. The subjects were 24 unproduced women. No gynecological diseases, no oral contraceptives or birth control rings. Pelvic examination is normal. Thirteen women in the dysmenorrheal group sought medical treatment from teens who were unable to work because of severe dysmenorrhea. No response to mild analgesics such as Paracetamol or aspirin. 11 controls were at least mild discomfort, seldom used analgesics. The general characteristics of the two groups no significant difference. Menstrual fluid is collected daily in a contraceptive diaphragm, and after three hours the diaphragm is removed and the volume measured. PGF 2α and PGE 2 in menstrual fluid were extracted by the previously described method.