Regional pulmonary blood flow during acute pulmonary edema: a PET study.

Regional pulmonary blood flow during acute pulmonary edema: a PET study.
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急性肺水肿期间的局部肺血流量:PET 研究。

DOI:
10.1152/jappl.1990.69.1.353
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发表时间:
1990
期刊:
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子:
--
通讯作者:
Haller,J
Haller,J
中科院分区:
--
文献类型:
--
作者:
Schuster,DP;Haller,J

文献摘要

被引文献

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本文应用正电子发射断层扫描(PET)技术,观察了硝普钠或前列环素(NP/Prost)对21只犬油酸(OA)致急性肺水肿后局部肺血流量(rPBF)的影响,并与11只单纯OA组和5只OA后给予甲氨蝶呤组的结果进行了比较。仅OA后,rPBF进行性降低发生在水肿的重力依赖性肺区域,但仅在11只狗中的6只。在这6只犬中,与基线或其他5只犬(3 +/- 19%)相比,rPBF下降41 +/- 12%(P <0.05)。在NP/Prost组中,血管扩张剂未能逆转OA后rPBF的任何变化,但确实防止了额外的去募集,直到药物输注停止,之后水肿区域的rPBF进一步下降。相比之下,OA后的甲氨蝶呤暂时加速,但没有定量增加水肿肺区域的rPBF减少。因此,在该模型中,水肿肺区域中的血管仅在去募集之前保持血管反应性。我们推测去募集的机制涉及水肿积聚和血管收缩之间的相互作用,其中肺损伤后rPBF的实际模式代表了负责血管去募集和前列环素产生的血管舒张机制之间的平衡。
We used positron emission tomography to evaluate the effects of nitroprusside or prostacyclin (NP/Prost) on regional pulmonary blood flow (rPBF) in 21 dogs after oleic acid- (OA) induced acute pulmonary edema and compared the results with data from 11 dogs given OA only and 5 given meclofenamate after OA. After OA only, a progressive decrease in rPBF occurred in edematous gravity-dependent lung regions, but only in 6 of 11 dogs. In these six dogs, rPBF fell 41 +/- 12% compared with base line or with the other five dogs (3 +/- 19%) (P less than 0.05). In the NP/Prost group, the vasodilators failed to reverse any change in rPBF after OA but did prevent additional derecruitment until the drug infusion was stopped, after which rPBF to the edematous regions decreased further. In contrast, meclofenamate after OA temporally accelerated but did not quantitatively enhance rPBF reduction in edematous lung regions. Thus, in this model, vessels in edematous lung regions remain vasoreactive only until derecruited. We speculate that the mechanism of derecruitment involves an interaction between edema accumulation and vasoconstriction, in which the actual pattern of rPBF after lung injury represents a balance between mechanisms responsible for vascular derecruitment and vasodilation from prostacyclin production.