Phorbol myristate acetate-induced injury of isolated perfused rat lungs: neutrophil dependence.
Phorbol myristate acetate-induced injury of isolated perfused rat lungs: neutrophil dependence.
复制标题
佛波醇肉豆蔻酸酯醋酸酯诱导的离体灌注大鼠肺损伤：中性粒细胞依赖性。
DOI：
10.1152/jappl.1988.65.5.2164
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Taylor,AE
中科院分区：
文献类型：
--
作者：
Perry,M;Taylor,AE
在离体灌注大鼠肺中研究了白细胞耗竭对静脉或气管内给药肉豆蔻酸酯磷酯（PMA）引起的急性肺损伤的影响。血管内皮通透性通过毛细管过滤系数（Kf,c）评估。预测肺毛细血管压力（Ppc,p）由测量毛细血管后阻力计算。这些参数分别在给药前和给药后90分钟（气管内或血管内）测量。当气管内和血管内均存在血元素时，Kf升高，c分别为0.27 +/- 0.02比0.99 +/- 0.22和0.25 +/- 0.05比0.64 +/- 0.15 (SE) ml.min-1. cmh20 -1.100 g-1；P < 0.05]， Ppc升高，P（分别为8.3 +/- 0.4 vs. 74.7 +/- 18.3和8.7 +/- 0.8 vs. 74.2 +/- 25.1 cmH2O, P < 0.05）。当气管内（0.35 +/- 0.06 vs. 0.23 +/- 0.07 ml.min-1. cmh20 -1.100 g-1）或血管内（0.39 +/- 0.07 vs. 0.33 +/- 0.07 ml.min-1. cmh20 -1.100 g-1）给予PMA时，循环白细胞的清除消除了升高的Kf，c。在无中性粒细胞的情况下，Ppc，p随气管内PMA轻微升高，从6.9 +/- 0.5到10.5 +/- 1.1 cmH2O (p < 0.05)，但在血管内PMA 90分钟时没有变化。用抗中性粒细胞血清去除循环中性粒细胞不能阻断Kf，c随气管内PMA的变化（从0.24 +/- 0.03到0.42 +/- 0.09 ml.min-1. cmh20 -1.100 g-1; P < 0.05）。Ppc、p也由6.9 +/- 0.6增加到19.8 +/- 6.7 cmH2O （p < 0.05）。（摘要删节250字）
he effect of leukocyte depletion on acute lung injury produced by intravenous or intratracheal phorbol myristate acetate (PMA) administration was studied in isolated perfused rat lungs. Vascular endothelial permeability was assessed by use of the capillary filtration coefficient (Kf,c). A predicted pulmonary capillary pressure (Ppc,p) was calculated from measurements of postcapillary resistances. These parameters were measured before and 90 min after the administration of PMA, either intratracheally or intravascularly. When blood elements were present both intratracheal and intravascular PMA caused an increased Kf,c [0.27 +/- 0.02 vs. 0.99 +/- 0.22 and 0.25 +/- 0.05 vs. 0.64 +/- 0.15 (SE) ml.min-1.cmH2O-1.100 g-1, respectively; P less than 0.05] and an increased Ppc,p (8.3 +/- 0.4 vs. 74.7 +/- 18.3 and 8.7 +/- 0.8 vs. 74.2 +/- 25.1 cmH2O, respectively; P less than 0.05). Removal of circulating leukocytes abolished the increased Kf,c when PMA was given intratracheally (0.35 +/- 0.06 vs. 0.23 +/- 0.07 ml.min-1.cmH2O-1.100 g-1) or intravascularly (0.39 +/- 0.07 vs. 0.33 +/- 0.07 ml.min-1.cmH2O-1.100 g-1). In the absence of neutrophils, Ppc,p slightly increased with intratracheal PMA, from 6.9 +/- 0.5 to 10.5 +/- 1.1 cmH2O (P less than 0.05), but was unchanged at 90 min with intravascular PMA. Depletion of circulating neutrophils with an antineutrophil serum failed to block the Kf,c change with intratracheal PMA (from 0.24 +/- 0.03 to 0.42 +/- 0.09 ml.min-1.cmH2O-1.100 g-1; P less than 0.05). Ppc,p also increased from 6.9 +/- 0.6 to 19.8 +/- 6.7 cmH2O (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)