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合成孕激素醋酸氯地孕酮对恢复慢性阻塞性肺疾病受损负荷代偿的作用。

Effect of chlormadinone acetate, a synthetic progesterone, on restoring impaired load compensation in chronic obstructive pulmonary disease.

作者信息

Kimura H, Tatsumi K, Kuriyama T, Sugita T, Watanabe S, Nishibayashi Y, Honda Y

出版信息

Tohoku J Exp Med. 1986 Jun;149(2):119-32. doi: 10.1620/tjem.149.119.

Abstract

We examined whether or not progestational agents can improve the pathophysiological conditions by augmenting the respiratory drives in chronic obstructive pulmonary disease (COPD). At first, respiratory drives evaluated by ventilation and occlusion pressure responses to CO2 with and without inspiratory flow-resistive loading were compared between 19 COPD and 21 control subjects. Although there were no significant differences in occlusion pressure responses to CO2 between both groups, the load compensation assessed by the ratio of loaded to unloaded slopes in the occlusion pressure response to CO2 was significantly lower in the COPD patients than in the control subjects. Secondly, 14 COPD patients administered chlormadinone acetate (CMA), a synthetic progesterone, were examined, and it was found that the patients restored the impaired load compensation, particularly significant in the bronchitic type. Thirdly, the ratio of ventilation to occlusion pressure response to CO2 (delta VI/delta P.2) was significantly decreased in the emphysematous type, whereas such was not the case in the bronchitic type. Thus, improvement of load compensation in the bronchitic type was considered to have been accomplished without accompanying an impairment of ventilatory efficiency. We conclude that CMA could be used as a relevant respiratory stimulant.

摘要

我们研究了孕激素类药物是否可通过增强慢性阻塞性肺疾病(COPD)患者的呼吸驱动来改善其病理生理状况。首先,比较了19例COPD患者和21例对照受试者在有和无吸气气流阻力负荷情况下,通过对二氧化碳的通气和阻断压力反应评估的呼吸驱动。尽管两组对二氧化碳的阻断压力反应无显著差异,但COPD患者中通过二氧化碳阻断压力反应中加载与未加载斜率之比评估的负荷补偿显著低于对照受试者。其次,对14例服用合成孕激素醋酸氯地孕酮(CMA)的COPD患者进行了检查,发现患者恢复了受损的负荷补偿,在支气管炎型患者中尤为显著。第三,肺气肿型患者中通气与二氧化碳阻断压力反应之比(δVI/δP.2)显著降低,而支气管炎型患者并非如此。因此,认为支气管炎型患者负荷补偿的改善是在不伴随通气效率受损的情况下实现的。我们得出结论,CMA可作为一种相关的呼吸兴奋剂。

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