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目的:探讨前列腺切除术后膀胱痉挛(BS)与前列环素水平的关系。方法:选择前列腺摘除术80例,于术前常规留取静脉血标本,通过测定炎性介质(6-K-PGF1α)反映前列环素(PGI2)水平,并于术后1～4天监测其水平变化,分析其与BS发作之间的关系。结果:术前6-K-PGF1α为(79.23±19.75)ng/L;术后共发生BS46例(57.5%),第1、2、3、4天6-K-PGF1α分别为(384.64±167.37)ng/L、(280.22±135.76)ng/L、(141.11±154.56)ng/L和(115.20±121.12)ng/L;未发生BS34例6-K-PGF1α分别为(219.53±100.13)ng/L、(167.31±65.26)ng/L、(89.23±17.84)ng/L和(76.86±23.71)ng/L。两组比较,差异显著(P<0.05)。结论:前列腺切除术后体内产生过多PGI2可能是引发BS的分子学基础之一。
Objective: To investigate the relationship between bladder spasm (BS) and prostacyclin after prostatectomy. Methods: 80 cases of prostatectomy were selected. Venous blood samples were routinely collected before surgery. PGI2 level was measured by measuring inflammatory mediators (6-K-PGF1α), and the levels of PGI2 were monitored 1 to 4 days after operation Level changes, analyze the relationship between BS and seizures. Results: Preoperative 6-K-PGF1α was (79.23 ± 19.75) ng / L. There were 46 cases (57.5%) of BS after operation, 6-K-PGF1α (141.1 ± 154.56) ng / L and (115.20 ± 121.12) ng / L, respectively. The incidence of 6-K-PGF1α in non-BS34 cases was (219.53 ± 100.13) ng / L, (167.31 ± 65.26) ng / L, (89.23 ± 17.84) ng / L and (76.86 ± 23.71) ng / L, respectively. The difference between the two groups was significant (P <0.05). CONCLUSIONS: Excess PGI2 produced in vivo after prostatectomy may be one of the molecular foundations of BS initiation.