Antibody-mediated neutrophil depletion preserves pulmonary vasomotor function.
Antibody-mediated neutrophil depletion preserves pulmonary vasomotor function.
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抗体介导的中性粒细胞耗竭保留了肺血管舒缩功能。
DOI：
10.1006/jsre.1996.0176
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Fullerton,DA
中科院分区：
文献类型：
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作者：
Sheridan,BC;McIntyreJr,RC;Meldrum,DR;ClevelandJr,JC;Agrafojo,J;Eisenach,JH;Harken,AH;Fullerton,DA
中性粒细胞耗竭通常用于检查中性粒细胞在肺损伤中的作用。然而，中性粒细胞耗竭本身对肺血管平滑肌松弛机制的影响尚不清楚。本研究的目的是检查中性粒细胞减少对cGMP介导的肺血管舒张的以下机制的影响：（1）受体依赖性内皮依赖性舒张（对乙酰胆碱（ACh）的反应），（2）受体非依赖性内皮依赖性舒张（对钙离子载体A23187的反应），和（3）内皮非依赖性舒张（对硝普钠（SNP）的反应）。在5只大鼠的肺收获前24小时，用抗中性粒细胞抗体血清诱导中性粒细胞增多（<75中性粒细胞/μl）。注射生理盐水的大鼠为对照组（n= 5）。ACh，A23187，和SNP的剂量反应曲线产生在离体肺动脉环预缩苯肾上腺素。采用单因素方差分析和事后Bonferroni-Dunn检验进行统计学比较，P < 0.05为显著性。ACh，A23187，和SNP的放松是完全在控制和血小板减少大鼠。因此，抗体介导的消耗不损害内皮依赖性或非依赖性cGMP介导的肺血管舒张。
Neutrophil depletion is commonly used to examine the role of neutrophils in lung injury. However, the effect of neutrophil depletion per se on mechanisms of pulmonary vascular smooth muscle relaxation is unknown. The purpose of this study was to examine the effect of neutropenia on the following mechanisms of cGMP-mediated pulmonary vasorelaxation: (1) receptor-dependent endothelium-dependent relaxation (response to acetylcholine (ACh)), (2) receptor-independent endothelium-dependent relaxation (response to the calcium ionophore A23187), and (3) endothelium-independent relaxation (response to sodium nitroprusside (SNP)). Neutropenia (<75 neutrophils/μl) was induced with anti-neutrophil antibody serum 24 hr prior to lung harvest in five rats. Saline-injected rats were controls (n= 5). Dose–response curves to ACh, A23187, and SNP were generated in isolated pulmonary artery rings preconstricted with phenylepherine. Statistical comparison was performed using one-way ANOVA with post-hoc Bonferroni–Dunn, andP< 0.05 was accepted as significant. Relaxation to ACh, A23187, and SNP was complete in both control and neutropenic rats. Thus, antibody-mediated depletion does not impair endothelial-dependent or -independent cGMP-mediated pulmonary vasorelaxation.