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离体犬肺中化学损伤与高血管压力损伤的相互作用

Interaction of chemical and high vascular pressure injury in isolated canine lung.

作者信息

Townsley M I, Lim E H, Sahawneh T M, Song W

机构信息

Department of Physiology, University of South Alabama, Mobile 36688.

出版信息

J Appl Physiol (1985). 1990 Nov;69(5):1657-64. doi: 10.1152/jappl.1990.69.5.1657.

DOI:10.1152/jappl.1990.69.5.1657
PMID:2272958
Abstract

Because both chemical and mechanical insults to the lung may occur concomitantly with trauma, we hypothesized that the pressure threshold for vascular pressure-induced (mechanical) injury would be decreased after a chemical insult to the lung. Normal isolated canine lung lobes (N, n = 14) and those injured with either airway acid instillation (AAI, n = 18) or intravascular oleic acid (OA, n = 25) were exposed to short (5-min) periods of elevated venous pressure (HiPv) ranging from 19 to 130 cmH2O. Before the HiPv stress, the capillary filtration coefficient (Kf,c) was 0.12 +/- 0.01, 0.27 +/- 0.03, and 0.31 +/- 0.02 ml.min-1.cmH2O-1 x 100 g-1 and the isogravimetric capillary pressure (Pc,i) was 9.2 +/- 0.3, 6.8 +/- 0.5, and 6.5 +/- 0.3 cmH2O in N, AAI, and OA lungs, respectively. However, the pattern of response to HiPv was similar in all groups: Kf,c was no different from the pre-HiPv value when the peak venous pressure (Pv) remained less than 55 cmH2O, but it increased reversibly when peak Pv exceeded 55 cmH2O (P less than 0.05). The reflection coefficient (sigma) for total proteins measured after pressure exposure averaged 0.60 +/- 0.03, 0.32 +/- 0.04, and 0.37 +/- 0.09 for N, AAI, and OA lobes respectively. However, in contrast to the result expected if pore stretching had occurred at high pressure, in all groups the sigma measured during the HiPv stress when Pv exceeded 55 cmH2O was significantly larger than that measured during the recovery period.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

由于肺部的化学性和机械性损伤可能与创伤同时发生,我们推测在肺部受到化学损伤后,血管压力诱导(机械性)损伤的压力阈值会降低。将正常离体犬肺叶(N组,n = 14)以及气道滴注酸(AAI组,n = 18)或血管内注入油酸(OA组,n = 25)损伤后的肺叶暴露于19至130 cmH₂O的短时间(5分钟)静脉压升高(HiPv)状态。在HiPv应激前,N组、AAI组和OA组肺叶的毛细血管滤过系数(Kf,c)分别为0.12±0.01、0.27±0.03和0.31±0.02 ml·min⁻¹·cmH₂O⁻¹×100 g⁻¹,等重力毛细血管压力(Pc,i)分别为9.2±0.3、6.8±0.5和6.5±0.3 cmH₂O。然而,所有组对HiPv的反应模式相似:当峰值静脉压(Pv)保持低于55 cmH₂O时,Kf,c与HiPv前的值无差异,但当峰值Pv超过55 cmH₂O时,Kf,c可逆性增加(P<0.05)。压力暴露后测量的总蛋白反射系数(σ)在N组、AAI组和OA组肺叶中分别平均为0.60±0.03、0.32±0.04和0.37±0.09。然而,与高压下发生孔扩张时预期的结果相反,在所有组中,当Pv超过55 cmH₂O时HiPv应激期间测量的σ显著大于恢复期测量的σ。(摘要截断于250字)

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