Academic Unit of Diabetes, Endocrinology & Metabolism, The University of Sheffield, Sheffield, UK.
J Endocrinol Invest. 2009 Oct;32(9):718-23. doi: 10.1007/BF03346526.
Testosterone is recognized to elicit vasodilatation in numerous vascular beds, however to date no study has investigated whether testosterone has this effect in the human pulmonary vasculature.
To determine whether isolated human pulmonary arteries and veins dilate in response to testosterone and whether the response differs in relation to gender, endothelial function or location with the pulmonary vasculature.
Intralobar pulmonary arteries [no.=44, diameter =581 (349) microm] and veins [no.=27, diameter =573 (302) microm] were dissected from lobectomy samples obtained from male and female patients [no.=40, age =69 (8) yr]. Vessels were mounted in an automated wire myograph, bathed in physiological saline at 37 C and pH 7.4, and loaded to their in vivo pressure. Vessels were preconstricted with noradrenaline (10 microM) and exposed to acetylcholine (1 microM) to assess endothelial function, washed and then preconstricted with potassium chloride (1-100 mM) followed by either cumulative concentrations of testosterone (1 nM-100 microM) or ethanol vehicle (<0.1%).
Significant marked vasodilatation was seen in all vessels, irrespective of size, gender and endothelial function at micromolar concentrations. Testosterone triggered significant vasodilatation at concentrations > or = 10 nM in pulmonary arteries obtained from males, a response which was not observed in vessels from females. The maximal response at 100 microM was also significantly greater in male pulmonary arteries. Significant vasodilatation was only observed at physiological (nM) concentrations in pulmonary resistance arteries and pulmonary arteries with good endothelial function.
Testosterone acts as an efficacious vasodilator in the human pulmonary vasculature, with dilatation observed at physiological concentrations in the male arterial resistance bed, dependent on the presence of an intact endothelium.
睾酮被认为可使许多血管床的血管扩张，但迄今为止，尚无研究调查睾酮是否对人体肺血管有这种作用。
确定分离的人肺动、静脉是否对睾酮产生舒张反应，以及这种反应是否因性别、内皮功能或肺血管位置而不同。
从男性和女性患者（n=40，年龄=69（8）岁）的肺叶切除术标本中分离出肺叶内肺动脉[n=44，直径=581（349）μm]和肺静脉[n=27，直径=573（302）μm]。血管在自动测径仪上进行测量，在 37°C 和 pH 7.4 的生理盐水中进行孵育，并在体内压力下进行负载。用去甲肾上腺素（10μM）预收缩血管，用乙酰胆碱（1μM）评估内皮功能，清洗后用氯化钾（1-100mM）预收缩，然后用睾酮（1nM-100μM）或乙醇载体（<0.1%）进行累积浓度处理。
所有大小、性别和内皮功能的血管在微摩尔浓度下均可见显著的舒张。睾酮在男性肺动中引起浓度>或=10nM的显著舒张反应，而女性血管中未观察到这种反应。在 100μM 时，最大反应也显著大于男性肺动。只有在生理浓度（nM）时才观察到肺阻力血管和内皮功能良好的肺动发生显著舒张。
睾酮在人体肺血管中作为一种有效的血管舒张剂，在男性动脉阻力床中观察到生理浓度下的舒张作用，且依赖于完整的内皮。
