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完整犬体内低氧性肺血管收缩与动脉血氧张力之间的关系。

The relationship between hypoxic pulmonary vasoconstriction and arterial oxygen tension in the intact dog.

作者信息

Orchard C H, Sanchez de Leon R, Sykes M K

出版信息

J Physiol. 1983 May;338:61-74. doi: 10.1113/jphysiol.1983.sp014660.

Abstract

The relationship between the magnitude of hypoxic pulmonary vasoconstriction (h.p.v.) and arterial oxygen tension (Pa,O2) has been studied in intact anaesthetized dogs. Radioactive 133Xe was infused continuously into the inferior vena cava. A tracheal divider made it possible to vary the inspired gas composition to each lung independently. With constant ventilation the 133Xe in the mixed expired gas from each lung was proportional to the blood flow to that lung. Unilateral ventilation of the left lung with 7% oxygen produced a diversion of blood flow away from the lung and a reduction in Pa,O2. Repeated hypoxic stimuli produced a progressively greater reduction in the blood flow to the hypoxic lung and a progressive increase in Pa,O2. Administration of a beta-adrenergic agonist, dobutamine hydrochloride, during ventilation of the left lung with 7% oxygen, resulted in an increased blood flow to the left lung and a further decrease in Pa,O2. Addition of CO2 to the inspired gas resulted in an increased diversion of blood flow away from the hypoxic lung but a decrease in Pa,O2. Respiratory alkalosis induced by over-ventilation decreased the hypoxic vasoconstriction and increased Pa,O2 slightly. However acid-base changes induced by infusion of 1 N-lactic acid or 8.4% NaHCO3 had no significant effects on the magnitude of the hypoxic vasoconstriction, or on Pa,O2, during hypoxic ventilation of the left lung. The magnitude of hypoxic vasoconstriction and Pa,O2 in the experiments described in 3, 4 and 5 above were positively correlated (r = 0.885), showing that the vasoconstriction may help to maintain Pa,O2. It is suggested that the effects of CO2 on h.p.v. and Pa,O2 may be explained largely by the changes in alveolar oxygen pressure (PA,O2) which are secondary to changes in PA,CO2.

摘要

在完整的麻醉犬身上研究了缺氧性肺血管收缩(h.p.v.)的程度与动脉血氧张力(Pa,O2)之间的关系。放射性133Xe持续注入下腔静脉。气管分隔器使独立改变每侧肺的吸入气体成分成为可能。在恒定通气情况下,来自每侧肺的混合呼出气体中的133Xe与该侧肺的血流量成正比。用7%氧气对左肺进行单侧通气会导致血流从该肺分流以及Pa,O2降低。重复的缺氧刺激使流向缺氧肺的血流量逐渐减少,而Pa,O2逐渐升高。在用7%氧气对左肺通气期间给予β-肾上腺素能激动剂盐酸多巴酚丁胺,导致左肺血流量增加而Pa,O2进一步降低。向吸入气体中添加二氧化碳会导致血流从缺氧肺的分流增加,但Pa,O2降低。过度通气引起的呼吸性碱中毒会降低缺氧性血管收缩并使Pa,O2略有升高。然而,在左肺缺氧通气期间,输注1N乳酸或8.4%碳酸氢钠引起的酸碱变化对缺氧性血管收缩的程度或Pa,O2没有显著影响。上述3、4和5中所述实验中缺氧性血管收缩的程度与Pa,O2呈正相关(r = 0.885),表明血管收缩可能有助于维持Pa,O2。有人认为,二氧化碳对h.p.v.和Pa,O2的影响很大程度上可能由肺泡氧分压(PA,O2)的变化来解释,而这种变化是PA,CO2变化的继发结果。

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