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阻塞后肺血管病中支气管侧支血管微穿刺压力

Bronchial collateral vessel micropuncture pressure in postobstructive pulmonary vasculopathy.

作者信息

Kelly S M, Taylor A E, Michel R P

机构信息

Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada.

出版信息

J Appl Physiol (1985). 1992 Nov;73(5):1914-24. doi: 10.1152/jappl.1992.73.5.1914.

Abstract

Postobstructive pulmonary vasculopathy, produced by chronic ligation of one pulmonary artery, markedly increases bronchial blood flow. Previously, using arterial and venous occlusion, we determined that bronchial collaterals enter the pulmonary circuit at the distal end of the arterial segment. In this study, we tested the hypothesis that pressure in bronchial collaterals (Pbr) closely approximates that at the downstream end of the arterial segment (Pao). We pump perfused [111 +/- 10 (SE) ml/min] left lower lobes of seven open-chest live dogs 3-15 mo after ligation of the left main pulmonary artery. Bronchial blood flow was 122 +/- 16 ml/min. We measured pulmonary arterial and venous pressures and, by arterial and venous occlusion, respectively, Pao and the pressure at the upstream end of the venous segment (Pvo). Pbr was obtained by micropuncture of 34 pleural surface bronchial vessels 201 +/- 16 microns in diameter. We found that Pbr (14.4 +/- 1.0 mmHg) was similar to Pao (15.0 +/- 0.8 mmHg) but differed significantly (P < 0.01) from Pvo (11.3 +/- 0.5 mmHg). In addition, Pbr was independent of systemic arterial pressure and bronchial vessel diameter. Light and electron microscopy revealed that, in the lobes with the ligated pulmonary artery, the new bronchial collaterals entered the thickened pleura from the parenchyma via either bronchovascular bundles or interlobular septa and had sparsely muscularized walls. We conclude that, in postobstructive pulmonary vasculopathy, bronchial collateral pressure measured by micropuncture is very close to the pressure in precapillary pulmonary arteries and that most of the pressure drop in the bronchial collaterals occurs in vessels > 350 microns in diameter.

摘要

由一侧肺动脉慢性结扎所导致的梗阻后肺血管病,可显著增加支气管血流。此前,我们通过动脉和静脉阻断法确定,支气管侧支在动脉段远端进入肺循环。在本研究中,我们检验了以下假设:支气管侧支压力(Pbr)与动脉段下游端压力(Pao)密切相近。我们对7只开胸活体犬在结扎左主肺动脉3至15个月后,以[111±10(标准误)毫升/分钟]的流量灌注左下叶。支气管血流为122±16毫升/分钟。我们测量了肺动脉压和肺静脉压,并分别通过动脉和静脉阻断法测量Pao以及静脉段上游端压力(Pvo)。Pbr通过对34条直径为201±16微米的胸膜表面支气管血管进行微穿刺获得。我们发现Pbr(14.4±1.0毫米汞柱)与Pao(15.0±0.8毫米汞柱)相似,但与Pvo(11.3±0.5毫米汞柱)有显著差异(P<0.01)。此外,Pbr与体动脉压和支气管血管直径无关。光镜和电镜检查显示,在结扎肺动脉的肺叶中,新的支气管侧支通过支气管血管束或小叶间隔从实质进入增厚的胸膜,且其壁肌肉化稀疏。我们得出结论,在梗阻后肺血管病中,通过微穿刺测量的支气管侧支压力非常接近肺毛细血管前动脉压力,并且支气管侧支中的大部分压力降发生在直径>350微米的血管中。

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