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前列腺素与非妊娠子宫。原发性痛经的病理生理学。

Prostaglandins and the non-pregnant uterus. The pathophysiology of primary dysmenorrhea.

作者信息

Pulkkinen M O

出版信息

Acta Obstet Gynecol Scand Suppl. 1983;113:63-7. doi: 10.3109/00016348309155200.

Abstract

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.

摘要

原发性痛经的生化背景特征为子宫前列腺素水平升高、血中精氨酸加压素水平升高以及月经周期后期雌二醇水平升高。在痛经患者中,出血开始时孕酮水平略高于月经正常者,但在月经周期后期则正常。生化作用通过游离的“激活剂”钙进行,这与可能的微观解剖学变化(如缝隙连接频率增加)一起,解释了平滑肌功能障碍。子宫活动的特征是传导速度高(由主动压力的高上升速率表明)和静息压力高。原发性痛经的病理生理学包括子宫血流减少和缺氧性疼痛,这是由子宫动脉收缩和/或子宫肌肉自身挛缩导致的。

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