雌二醇对离体和在体气管平滑肌收缩活动的抑制作用

目的:研究雌二醇对离体和在体气管平滑肌收缩的作用.方法:(1)将家兔离体气管平滑肌条置于装有Krebs液的肌槽中温育,并通入95％O_2和5％CO_2的混合气体.二导记录仪记录肌条的等长张力.(2)测量肌注雌二醇(1mg/kg)前后乙酰胆碱和组胺引发豚鼠哮喘的潜伏期.结果:(1)雌二醇(100μmol/L)对乙酰胆碱和氯化钾诱发的收缩有明显的舒张作用(舒张百分比分别为39％±5％和45％±19％).其作用可被蚓哚美辛和亚甲蓝部分阻断(26％±8％和28％±13％),但不能被L-NNA、心得安和去除上皮所影响(舒张百分比分别为38％±10％,40％±15％,37％±8％).雌二醇能使乙酰胆碱及氯化钙的量效曲线明显右移(pD_2~′值分别为3.98和4.75).另外,雌二醇可明显抑制乙酰胆碱引起的第Ⅰ时相性收缩,对氯化钙引起的第Ⅱ时相性的收缩无明显影响.(2)肌注雌二醇(1mg/kg)可使豚鼠的引喘潜伏期明显延长.结论:(1)雌二醇对兔离体气管平滑肌的作用是非上皮依赖性的,与抑制电压依赖性钙通道和细胞内钙从内质网的释放有关,还部分与cGMP介导的松弛途径及刺激气道平滑肌释放前列腺素类物质有关,但与β-肾上腺素能受体介导的舒张无关.(2)雌二醇可明显舒张豚鼠在体气管平滑肌.

Inhibition of beta-estradiol on trachea smooth muscle contraction in vitro and in vivo

AIM: To investigate the effect of beta-estradiol on trachea smooth muscle contraction in vitro and in vivo. METHODS: (1) Rabbit tracheas were incubated in organ baths filled with Krebs solution and supplied with a mixed gas of 95 % O2 and 5 % CO2. The isometric force was measured by ink-writing recorders. (2) The incubation period of asthma induced by histamine and acetylcholine (ACh) in guinea pig were measured before and after beta-estradiol (1 mg/kg) were given intramuscularly. RESULTS: (1) Administration of beta-estradiol (0.1 mmol/L) caused relaxation of isolated trachea muscle strips (TMS) in rabbits pre-contracted by ACh and KCl (39 % +/- 5 % and 45 % +/- 19 %). The presence of indomethacin or methylene blue partly decreased the relaxation to beta-estradiol (26 % +/- 8 % and 28 % +/- 13 %), but Nomega-nitro-L-arginine (L-NNA) and propranolol and epithelium removal did not affect it (38 % +/- 10 %, 40 % +/- 15 %, 37 % +/- 8 %). beta-Estradiol can shifted the concentration-response curves of ACh and CaCl2 to the rightward (pD2 = 3.98 and 4.75). In addition, it could also significantly inhibit the contraction of phase caused by ACh, but did not affect the contraction of phase II caused by CaCl2. (2) The incubation period of asthma in guinea pig were delayed by beta-estradiol (1 mg/kg) given intramuscularly. CONCLUSION: (1) The relaxation of beta-estradiol in vitro was epithelium independent and associated with the inhibition of potential-dependent channel and release of Ca2+ from sarcoplasm reticulum induced by ACh. In addition, release of prostaglandins from trachea smooth muscle cells and relaxation through cGMP approach were also included. beta-Adrenoceptor-mediated relaxation was not involved. (2) beta-Estradiol can relax the trachea in vivo in guniea pig.