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原发痛经病因可分为内分泌性、子宫肌性、前列腺素(PGs)、宫颈性及心理性五大类。现认为后两种不是主要病因而为反应性现象。至于内分泌因素,因无排卵即无原发痛经,故排卵及雌、孕激素对子宫内膜与肌层的作用为主要机制。最近提出血管加压素升高亦为病因之一,有待进一步研究。在绝大多数患者中可见子宫收缩力异常升高,常继发于来自内膜过量的PG作用。原发痛经有四项主要异常所见:即子宫肌层静止张力升高大于10mmHg,子宫肌层收缩压升高至120mmHg以上,收缩频率增加以及节律紊乱,导致子宫血流减少和缺氧,内膜释放PG增多而致腹痛。绝大多数非甾体抗炎药物(NSAIDs)为PG合成酶抑制剂,主要作用是阻断环氧合酶通路。孕
The primary cause of dysmenorrhea can be divided into endocrine, uterine muscle, prostaglandin (PGs), cervical and psychological five categories. Now that the latter two are not the main cause but a reactive phenomenon. As for the endocrine factors, that is, no anovulatory dysmenorrhea, ovulation and estrogen and progesterone on the role of endometrial and muscular layer as the main mechanism. Recently, it is also suggested that the increase of vasopressin is one of the causes for further study. Abnormal uterine contractility can be seen in the vast majority of patients, often secondary to intimal hyperplasia of PG. There are four main abnormalities seen in the primary dysmenorrhea: the myometrium more than 10mmHg static tension, myometrial systolic blood pressure increased to 120mmHg or more, increased frequency of contraction and rhythm disorders, leading to uterine blood flow reduction and hypoxia, within Increased membrane release of PG caused by abdominal pain. The vast majority of non-steroidal anti-inflammatory drugs (NSAIDs) are PG synthetase inhibitors, the main role is to block the cyclooxygenase pathway. pregnant