内皮细胞损伤对肺血管反应性的影响。

Effects of endothelial cell injury on pulmonary vascular reactivity.

作者信息

Rounds S, Farber H W, Hill N S, O'Brien R F

出版信息

Chest. 1985 Oct;88(4 Suppl):213S-216S. doi: 10.1378/chest.88.4_supplement.213s.

DOI:10.1378/chest.88.4_supplement.213s

Abstract

Using the thiocarbamide model of acute lung injury in rats, we found that alpha-naphthylthiourea (ANTU) caused lung endothelial cell injury, as evidenced by increased permeability edema and decreased angiotensin I conversion. These effects were associated with enhanced pulmonary vascular reactivity. Recurrent ANTU lung injury caused pulmonary hypertension. The water-soluble thiocarbamide thiourea caused cultured vascular endothelial cells to release neutrophil chemoattractant activity. We speculate that endothelial cell injury may modulate the function of vascular smooth muscle and blood leukocytes.

摘要

利用大鼠急性肺损伤的硫脲模型，我们发现α-萘基硫脲（ANTU）可导致肺内皮细胞损伤，表现为通透性水肿增加和血管紧张素I转化减少。这些效应与肺血管反应性增强有关。反复的ANTU肺损伤可导致肺动脉高压。水溶性硫脲可使培养的血管内皮细胞释放中性粒细胞趋化活性。我们推测内皮细胞损伤可能会调节血管平滑肌和血液白细胞的功能。