Forman A, Ulmsten U, Andersson K E
Acta Obstet Gynecol Scand Suppl. 1983;113:71-6. doi: 10.3109/00016348309155202.
Uterine hypercontractility is considered to be an important factor in primary dysmenorrhea. A survey is given on possible mechanisms controlling the cytoplasmic concentration of free calcium and thereby contractile activity in the myometrial smooth muscle cell. Probably acting by different modes of action, inhibitors of prostaglandin synthesis, calcium antagonists and beta 2 stimulators have all been shown to reduce myometrial activity and relieve dysmenorrheic pain. The possibility of achieving further uterine relaxation after initial treatment with prostaglandin inhibitors by adding a calcium antagonist such as nifedipine is discussed. It is also suggested that when utilizing a reliable pressure recording technique in the evaluation of dysmenorrheic patients, the pronounced myometrial relaxation obtained by such combined therapy may be of diagnostic value.
子宫收缩过强被认为是原发性痛经的一个重要因素。本文综述了控制子宫肌层平滑肌细胞内游离钙浓度从而调节收缩活性的可能机制。前列腺素合成抑制剂、钙拮抗剂和β2激动剂可能通过不同的作用方式，均已被证明可降低子宫肌层活性并缓解痛经。本文还讨论了在最初使用前列腺素抑制剂治疗后，加用钙拮抗剂（如硝苯地平）进一步松弛子宫的可能性。此外，本文还提出，在评估痛经患者时，若采用可靠的压力记录技术，这种联合治疗所获得的明显子宫肌层松弛可能具有诊断价值。
