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肺动脉扩张不会引起肺血管收缩。

Pulmonary arterial distension does not cause pulmonary vasoconstriction.

作者信息

Lloyd T C

出版信息

J Appl Physiol (1985). 1986 Aug;61(2):741-5. doi: 10.1152/jappl.1986.61.2.741.

Abstract

Distension of the main pulmonary artery or its major branches with an intraluminal balloon has been reported to cause pulmonary vasoconstriction by an unknown mechanism. This study was an attempt to confirm the pressor response and explore its cause. Several balloon distension methods were tried and discarded because they caused unintentional obstruction. Ultimately, I inflated a balloon placed retrogradely and confined to the left main pulmonary artery of six anesthetized open-chest dogs after ligating left lobar arterial branches. Blood flow and systemic gas composition were controlled by interposing an external pump oxygenator between the left ventricle and aorta. Pressures in the aorta, main pulmonary artery, and left atrium were recorded. Alveolar hypoxia was used as an independent test of pulmonary vasoreactivity. Although hypoxic pressor responses occurred, challenges with arterial distension did not change lung perfusion pressure. Silicone rubber casts were made of the arteries of six dogs used in pilot experiments. These revealed the limited lengths in which distenders can be placed without unintentional encroachment on flow. I could not support the conclusion that arterial distension causes vasoconstriction and am suspicious that the perfusion pressure increases reported by others may have been caused by undetected obstruction of a major arterial branch.

摘要

据报道,用腔内球囊扩张主肺动脉或其主要分支会通过一种未知机制导致肺血管收缩。本研究旨在证实这种升压反应并探究其原因。尝试了几种球囊扩张方法,但因会导致意外阻塞而被舍弃。最终,在结扎左叶动脉分支后,我对六只麻醉开胸犬的左主肺动脉逆行放置并限制在其中的一个球囊进行了充气。通过在左心室和主动脉之间插入一个外置泵氧合器来控制血流和全身气体成分。记录主动脉、主肺动脉和左心房的压力。使用肺泡低氧作为肺血管反应性的独立测试。尽管出现了低氧升压反应,但动脉扩张刺激并未改变肺灌注压。对用于前期实验的六只犬的动脉制作了硅橡胶铸型。这些铸型显示了在不意外侵犯血流的情况下可以放置扩张器的有限长度。我无法支持动脉扩张会导致血管收缩的结论,并且怀疑其他人报告的灌注压升高可能是由未检测到的主要动脉分支阻塞所致。

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